This article is a collaboration with Immunology Explained, an initiative by the American Association of Immunologists (AAI) to connect you to the science behind your health.

What is MCAS?

MCAS is a condition in which mast cells release chemical mediators inappropriately or excessively, leading to recurrent symptoms affecting multiple body systems. In MCAS, mast cells frequently release mediators in response to triggers that would not typically cause such a strong reaction. People with MCAS experience these overactive immune responses frequently and repeatedly, causing symptoms that have a substantial impact on their daily lives.

photo of a mast cell (center, dark purple) releasing chemical mediators from its intracellular granules upon activation (one example is histamine)

Living with MCAS - A Patient’s Story

We asked Jenna Gestetner, a young woman who lives with the diagnosis of MCAS herself to share her story to add her personal experience to the science behind MCAS. You can find her online @JennaXHealth

I (Jenna) was a seemingly healthy child. I’d get the “normal” sicknesses, but there was always something odd about them. I got ear infections, but abnormally often. I got shin splints from running track, but they were very hard to treat. By the time I was 12, the everyday symptoms started. Headaches. Stomach aches. Itching. Nausea. Dizziness. Fatigue. And so much more. When I’d tell anyone, they’d say, “Me too! I’m always tired, I always have a stomachache. It’s so annoying, right?” So, I assumed everyone felt this way.

Around the age of 12, things took a turn: I went from being able to eat every single food to slowly starting to react to them all. I soon realized a lot of my symptoms were caused by certain foods, so I’d stop eating them and feel better. A couple months later, the same thing would happen again. Over the past 12 years, this pattern has continued to happen. Today, I can only eat 9 foods. But it is not just food—I react to fabrics like linen, changes in pressure and temperature, and even my own sweat.

The scariest part is how unpredictable MCAS is. A food I’d eat one day that I’d been eating safely for months would, the next day, suddenly cause a severe reaction. When your own body can turn on something as ordinary as fabric or a change in pressure, you stop trusting that anything is safe.

When I’d go to my pediatrician and specialists, I’d check almost every box on the symptom checklist. But when I’d be asked specifics, it all blurred together and made my experience confusing and unproductive (something I can only describe as bleh). So, each specialist would take the symptom(s) that fell in their lane, run a test, and when it came back normal, it was dismissed. Insignificant. Nothing to worry about. It felt like it was concerning enough to warrant looking into but never amounted to enough that anyone had to do anything about it. I know now that my MCAS was hard to diagnose partly because doctors and researchers are still learning so much about it.

I’d been called “sensitive” my whole life, as if I just needed to be stronger to endure these interactions. The healthcare providers I saw told me many of my symptoms weren’t signs of a real condition, that I might never find an answer that explained everything. But deep down, I knew there was one.

It wasn’t until a particularly strange reaction where my doctor mentioned mast cells as a casual explanation that led me to discovering Mast Cell Activation Syndrome (MCAS). Learning more about it, every single little seemingly random health issue I’d had since the day I was born made sense. And it was all being caused by my immune system. I turned to the internet and read as much as I could find. Every odd problem I’d had that’d been called abnormal or not a significant issue was indicative of MCAS. Each new piece of information I gathered about MCAS explained another piece of my life. It was like finally being able to put together the puzzle of a bag of pieces I’d carried around my entire life.

Despite being sure I had found the answer I’d been searching for, getting a diagnosis was still far from easy. First, I had to find an allergy and immunology specialist who knew about MCAS, which was challenging back in 2020. Then, I had to find one that followed the newly published diagnostic criteria (because I didn’t meet the old one). Even then, getting an official diagnosis took persistence, creativity, and a lot of luck.

The amazing thing is that there are so many treatments for MCAS now. Medications and treatments recommended by my doctors have made a huge difference in certain symptoms. But each one only begins to scratch the surface of the ways in which this condition impacts my body and my life.

I’ve come to realize as much as this is physical, ultimately, it is a mental battle. Other people not understanding it, not believing it, or not having a name for it doesn’t make it any less real. It’s real because it is my experience. It is a battle to live my life despite the restrictions. Every day I must make decisions about what I can eat, what I can wear, where I can go—silently calculating every little thing. I have to simultaneously be vigilant, hold the fear of the next unpredictable reaction, and fight through the physical symptoms—all while resisting the urge to let it shrink my life. Health is just one part of life. The goal isn’t a perfectly fixed body, it’s to live a fulfilling life. So, that’s what I focus on. Much of the journey of having MCAS is unpredictable and out of your hands, but I’ve learned that happiness is shaped by your perception, and the power to create your perception is in your hands.

What are mast cells?

Mast cells are an important part of your immune system. They live in tissues throughout your body and patrol for things that shouldn’t be there. Mast cells help protect against parasites and toxins, aid in wound healing, and help coordinate immune responses by releasing chemicals that attract and activate other immune cells .

Mast cells are sometimes called the “allergy cell” because they are also responsible for immediate allergic reactions such as urticaria or hives. They play a central role in allergic responses by releasing chemicals called mediators, like histamine, in response to something otherwise harmless like pollen, pet dander, or food. The release of these mediators leads to common symptoms of allergies like runny noses, hives, and anaphylaxis.

How do mast cells work?

In allergic reactions, the immune system (B cells specifically) produces a type of antibody called IgE. IgE attaches to mast cells and acts like a sensor. When an allergen such as pollen or pet dander enters the body, the IgE ‘sensor’ on the mast cell recognizes the allergen and triggers mast cells to release their stored mediators, including histamine and tryptase. Activated mast cells can also make and release additional chemical mediators called leukotrienes, prostaglandins, and cytokines.

Think of this like a piñata. The piñata is the mast cell. The IgE bound to allergen is like the person holding the stick that hits the piñata, causing the release of candy. All the candy falling out of the piñata is like the mediators leaving the mast cell after being activated.

But allergens working though IgE aren’t the only way that mast cells can be activated. Mast cells also have sensors (known as receptors) for other proteins and chemical mediators produced during immune responses. They can also be activated by microbes, neurotransmitters, hormones, growth factors, and even some prescription medications and physical triggers like vibration. In patients dealing with mast cell activation symptoms, the release of mast cell mediators may be driven by any one of these factors.

How can mast cells become overactive?

Mast cells may become overactive due to a genetic mutation that directly changes the way the mast cells appear and behave. In people with clonal mast cell activation syndromes (also celled systemic mastocytosis and monoclonal mast cell activation syndrome, or cutaneous mastocytosis with systemic mast cell activation), this mutation makes the mast cells unstable and lowers the threshold for them to overreact to stimuli.

Other people may carry a genetic trait called hereditary alpha tryptasemia (HaT) that increases the amount of a specific mast cell mediator called tryptase in their bodies, which increases the chances of developing an overactive mast cell activation response and severe anaphylaxis, a rapid and life-threatening allergic reaction.

Others may have no known genetic differences that directly affect their mast cells or that increase their risk of severe anaphylaxis. For these patients, it is unclear what causes mast cells to have a lower threshold for spontaneous activation or for overactivity after exposure to a stimulus. Researchers are actively trying to understand what could drive spontaneous mast cell activation in people without clonal mast cell disorders or IgE-driven conventional allergies.

Symptoms of mast cell activation are also found in some individuals with hypermobile joints and other collagen or connective tissue differences. They may also be seen in people with neurologic problems, like autonomic nervous system dysfunction and pain syndromes. Researchers are still trying to understand why mast cells seem more ‘twitchy’ in these conditions and why the vast majority of people with mast cell activation and related conditions frequently don’t have positive laboratory testing needed to formally diagnose them with MCAS.

What happens when mast cells become overactive?

In MCAS, mast cells become unusually sensitive and release mediators too easily or too often. For lots of people with MCAS, it’s not just allergens that can cause mast cells to release mediators. Things like heat or cold, stress, exercise, drugs, food, beverages, and more, can activate mast cells. These responses are unpredictable and symptoms can vary. Each person’s triggers are unique and can change over time.

What makes MCAS different?

How is MCAS Different from Autoimmune Disease?

Autoimmune disorders occur when the immune system mistakenly attacks part of the body. In MCAS, the immune system is not directly attacking the body but rather overreacting to stimuli or spontaneously reacting. With MCAS, immune cell activation is deregulated.

How is MCAS Different from Allergies?

Many common allergic reactions are driven by IgE antibodies. After exposure to an allergen, your immune system (B cells specifically) creates IgE antibodies to “fight” the allergen if you are exposed again. Later exposures trigger mediator release when IgE binds to mast cells (described above). Most allergic reactions happen quickly after exposure and with consistent symptoms. In a classic type I hypersensitivity or IgE-mediated allergy response, it is often easy to identify the trigger, and the presence of IgE can test for allergies. While allergies and MCAS both involve mast cells, MCAS is characterized by inappropriate or excessive mast cell activation that can occur in response to many different triggers and doesn’t necessarily require IgE.

What are MCAS symptoms?

The symptoms of MCAS can be wide-ranging, including:

• Heart related symptoms:

• Rapid pulse (tachycardia)

• Low blood pressure (hypotension)

• Skin related:

• Itching

• Hives (urticaria)

• Swelling

• Skin turning red (flushing)

• Lung related:

• Wheezing

• Shortness of breath

• Trouble breathing and/or throat closing.

• Gastrointestinal related:

• Diarrhea

• Nausea with vomiting

• Crampy abdominal pain

Many symptoms of MCAS are linked to other common health conditions, making it difficult for some healthcare providers to connect them to MCAS.

How is MCAS Diagnosed?

There are three criteria that allergists/clinical immunologists use to diagnose MCAS.

1. Symptoms consistent with conventional allergic reactions that involve at least 2 out of the 4 organ systems listed: skin and mucus membranes; gastrointestinal tract, airways (nasal passages, ears, lungs); and cardiovascular (low blood pressure, fast heart rate, and symptoms that can go along with these signs like dizziness, lightheadedness, fainting, etc.), and that are severe and recurrent

2. Laboratory tests that indicate mast cell activation

3. Patients respond to medications that target mast cells or their mediators

Laboratory tests for MCAS include blood tests showing increases in tryptase or other mast cell mediators or urine tests showing increases in breakdown products of mast cell mediators. Laboratory tests can be difficult for a variety of reasons, including the need to be done just after a reaction when mediators are still present and that not all mediators can be easily tested for.

What Treatments are Available for MCAS?

Treatment for MCAS varies person to person based on their symptoms and experiences. Patients should work with their doctors to determine the best treatments for their particular symptoms and triggers. Some possible treatments include:

• Antihistamines to dampen allergy-like symptoms

• Epinephrine, like in an epi-pen, when a patient is experiencing anaphylaxis

• Aspirin to reduce flushing

• Leukotriene modifiers to help with breathing

• Mast cell stabilizers to prevent mediator release

• Omalizumab, a monoclonal antibody that blocks binding of IgE to mast cell receptors and has been reported to reduce mast cell reactivity and sensitivity to activation

• Corticosteroids to reduce inflammation

• Specific chemotherapy medications for patients with clonal mast cell disorders

What Researchers are Working to Figure Out

The truth is that there is still a lot we don’t know about MCAS. Researchers are working hard to understand what causes the disease and how it progresses to improve diagnostics and treatments.

There are many active areas of MCAS research, including:

• How genetics may play a role in MCAS

• How mast cells change in MCAS

• How to improve tests for various mediators

• How MCAS overlaps with other diseases

• New drugs to treat MCAS

Living with mast cell activation syndrome can be frustrating, unpredictable, and at times isolating. But as awareness grows and research advances, so does our ability to understand, manage, and support those affected. Every new discovery brings us one step closer to turning uncertainty into answers and helping people with MCAS live fuller, healthier lives.

Resources to learn more about MCAS:

Mast Cell Disease Society: https://tmsforacure.org/

The itch podcast: https://www.itchpodcast.com/episodes/63-mast-cell-disease

Dr. Kara Wada: https://www.drkarawada.com/post/mcas-vs-allergies-confusion

American Academy of Allergy, Asthma, and Immunology (AAAAI). Mast Cell Activation Syndrome (MCAS): https://www.aaaai.org/conditions-treatments/related-conditions/mcas

American Academy of Allergy, Asthma, and Immunology (AAAAI). MCAS, Evaluation and Diagnosis: https://www.aaaai.org/allergist-resources/ask-the-expert/answers/2022/mcas

AAAAI Podcast: Conversations from the World of Allergy - Unraveling Mast Cell Activation Syndrome: https://www.buzzsprout.com/2049216/episodes/17697879

It may seem trivial but say the word out loud and notice what your body does with it. Shot. The same word we use for gunfire, for something violent happening to a body against its will. Nobody’s brain hears “shot” and immediately relaxes. When a word carries that kind of baggage into a conversation about health, it’s already working against you before you’ve said anything else.

image from Vecteezy

That’s the premise of this post: in science communication, word choice isn’t frivolous. Word choice matters and it’s part of the science. Of course, the facts don’t change based on the words we use to describe them, but people’s willingness to hear those facts absolutely does. If we care about our audience actually understanding the science, we have to carefully choose the words we use when we describe the science.

Choosing “vaccine” instead of “shot”

Using the word “shot” is familiar, and everywhere, which is exactly why it’s worth interrogating. Words can inadvertently accumulate meaning from every other context they’re used in, and the word “shot” spends most of its life describing violence. That association doesn’t switch off just because we’re standing in a clinic or sharing the latest scientific evidence on new mRNA vaccines that prevent recurrence of melanoma or improve the annual influenza vaccine..

I’ve moved away from “shot” and toward “vaccination” or “immunization” instead. While neither word is exciting (and that’s the point), they describe what’s actually happening. Vaccination is a process that works with your immune system to prepare it and provide memory for later exposure with the real-life infectious pathogen. Vaccination is not an event that happens to you, it is an event that works with you (your immune system) and builds defense.

Choosing “infection immunity” over “natural immunity”

This is the framing I feel most strongly about, and the one I’d most like people to walk away from this post rethinking is “natural immunity.”

“Natural immunity” implies that immunity gained through infection is somehow more organic, more orderly and less harmful than immunity gained through vaccination. But that’s not how nature works. Both routes – immunity through infection and immunity from vaccination – teach your immune system using the exact same (dare I say natural) components of the immune system - T cells, B cells and resulting antibody. There is nothing unnatural about a vaccine-trained immune response; it is your own immune system doing exactly what it evolved to do.

The real difference between the two isn’t natural. It’s risk.

· Infection immunity is immunity built after your body fights off an actual pathogen after infection and is bundled with the disease itself. You don’t get to opt into just the immunity part. You take on fever, complications, hospitalization risk, long-term damage, and in some cases death, as the price of infection.

· Vaccine immunity is immunity built through guided exposure to a harmless version of the pathogen or the instructions to build a tiny piece of the pathogen. Vaccines train the same immune system as the infection would, using the same biological tools, but without the gamble. It’s an immune response that is guided, without the risk of the consequences of infection.

Calling one “natural” and leaving the other unnamed quietly tells people that infection is the default, honest way to become immune, and vaccination is some kind of workaround. That’s backwards. Both involve your immune system at work. One (infection) just asks you to bet your health to get there while the other (vaccine) guides you on a safer path to immunity.

So, in my own writing and talks, I’ve retired “natural immunity” altogether and use infection immunity and vaccine immunity side by side as parallel terms, for what -they are: two paths to the same biological outcome, with very different price tags.

Side note. You can read an entire article I wrote about it as a collaboration with Unbiased Science and the American Association of Immunologists (AAI) Immunology Explained website using the links below.

https://theunbiasedscipod.substack.com/cp/178205243

https://immunologyexplained.aai.org/news/vaccine-immunity-vs-infection-out-in-the-wild-whats-the-difference-and-why-it-matters/

Careful word selection is worth the effort

Would it be easier to continue to use the common words? Yes.

Will anyone accuse you of being unscientific for saying “shot” or “natural immunity”? No. They’re everywhere, including textbooks and excellent science writing.

But here in the business of science communication, we know that “easier” and “more accurate” aren’t the same thing. As science communicators, accuracy should include the emotional accuracy of our language, not just the technical accuracy of our facts. If the words we default to are quietly stacking the deck by making one option sound violent and the other sound wholesome, making one sound “natural” and the other sound artificial, then we are shaping the conclusion before the audience has even weighed the evidence.

A short list to get started

If you want to start paying attention to this in your own communication, a few places to look:

• Change the use of the word “shot” to vaccine or immunization

• Change the use of the word “natural immunity” to “infection immunity” (paired with “vaccine immunity”)

• Any term that implies one path is the “default” or “real” version of a biological process, when multiple paths lead to the same outcome

None of this is about softening the truth or being overly semantic with language for its own sake. It’s about noticing the implication of the words we choose and choosing, deliberately, to have them work for clarity instead of against it.

That’s the whole job, really. Not just knowing the science but saying it in words that don’t set off emotional alarm bells and let people actually hear it, opening the door to understanding and not defensiveness.

Thanks for being here :)

It’s become a tradition, and every year, something similar happens. Out of the eighty dental students in the room, about twenty-five walk out having registered as potential marrow donors. The whole ask includes a cheek swab, a quick survey and contact information. That’s it.

^ ^ ^ To read the full instagram story go to @funsizeimmuninja August 10, 2026 ^ ^ ^

Most of those students who register as donors will never get “the call.” The odds of any one person being a match for another is a long shot. But there’s a chance and for the patient on the other end of that call, it can be the only thing standing between them and a second chance at life.

Blood cancer doesn’t wait for a convenient time

Here’s the part that’s easy to forget when you’re swabbing your cheek in a lecture hall: the call doesn’t come on your schedule. It comes on the patients. It might come during finals or in the middle of starting a new job. It could come mid-move to a new city, mid-wedding-planning, or a month before graduation. There’s no good time for someone else’s cancer to become your emergency but that’s exactly the deal you sign up for when you join the registry. Not a guarantee you’ll be needed, just a promise that if you are, you’ll show up.

That’s what happened to one of my former students. AJ registered in my classroom 3 years ago, back when he was still a first-year dental student worrying about coursework, upcoming boards, and clinical rotations. Years later - exactly one month before graduating from dental school - he got the call and said “YES!”

Why this particular kind of generosity is so rare — and so needed

Matching for bone marrow and stem cell donation is far more specific than matching for a blood transfusion. It depends on human leukocyte antigen (HLA) typing, which are highly polymorphic (many forms) and inherited, which means patients are most likely to match with someone who shares their ethnic and genetic background. Patients from mixed-race backgrounds, and from Black, Hispanic, Asian, and Native American communities, often have the hardest time finding a match, simply because those groups are underrepresented on the registry.

That’s part of why NMDP keeps showing up in classrooms like mine. Every registrant, regardless of background, adds to the pool of possible matches. Some registrants will be the only match a particular patient ever finds. That’s where AJ came in. During one of the most chaotic times of his life, he cleared his calendar and flew across the country to donate a life-saving sample. I can honestly say I consider AJ to be a hero!

What joining the nmdp registry actually involves

• A cheek swab, done in a few minutes, either at an in-person drive (like my classroom) or a kit mailed to your home

• Updating your contact information so NMDP can reach you if you’re ever identified as a match

• Saying yes (or no — it’s always your choice) if that call ever comes

If you are matched, donation itself is usually done one of two ways: through a blood draw called PBSC (peripheral blood stem cell) donation, which is non-surgical and kind of like a lengthy blood draw, or, less commonly now, through a marrow donation from the back of the pelvic bone, done under anesthesia. Neither costs the donor anything financially as NMDP covers travel and expenses. Most donors are back to normal activities within a few days to a couple of weeks.

The registry costs you nothing. For the person waiting on a match, it can mean everything.

The ask

I’ll keep bringing NMDP reps into my classroom every year, and I’ll keep watching a quarter of the room walk out registered. But the registry needs more than dental students in Colorado.

If you’re between 18 and 40 (the age range NMDP prioritizes, since younger donors tend to produce better outcomes for patients), healthy, and willing, you can request a swab kit at nmdp.org. It takes less time than reading this article did.

You may never get the call. But if you do, you’ll be exactly the person someone else in need has been waiting for.

Learn more or join the registry at nmdp.org

Say the word “vaccine“ out loud, and watch what happens. Some people relax. Others tense up. Most land somewhere in between, with a bunch of lingering questions and half-remembered facts. Let’s skip the noise and get straight to the biology.

Vaccines Give Your Immune System a Practice Run

Think of your immune system as a highly trained security team. The moment an unfamiliar pathogen, like a virus or a bacterium, slips past your defenses, that team scrambles to figure out the threat. Sizing up a total stranger takes time. While your immune system is still gathering intel, you’re the one getting sick.

Vaccines close that gap. They introduce a harmless version or fragment of the pathogen — enough to be recognizable, not enough to make you ill. Your immune cells study it, learn to how defeat it, and file it away for later in the form of memory T, memory B cells and antibody. So, when the real pathogen eventually shows up, your body isn’t starting from scratch. It already knows exactly what to do.

Current types of vaccines approved in the U.S. and how they work:

Live-Attenuated Vaccines
Use weakened versions of pathogens so they can still replicate just enough to train the immune system but not cause illness. Often require fewer doses and provide long-lasting protection. Examples include MMR (measles, mumps, rubella), varicella (chickenpox), and yellow fever vaccines.

Inactivated (Killed) Vaccines
Use pathogens that have been inactivated (killed) so they cannot replicate. They provide a safe way to stimulate immunity, though multiple doses may be needed. Examples include inactivated flu shots, inactivated polio, hepatitis A, and rabies vaccines.

mRNA Vaccines
Use messenger RNA to instruct your cells to produce a harmless piece of a virus (i.e. the spike protein for SARS-CoV-2) triggering an immune response. The mRNA itself doesn’t enter the nucleus or alter DNA. Examples include Pfizer‑BioNTech (Comirnaty) and Moderna (Spikevax, mNexspike) COVID‑19 vaccines.

Future promise: Researchers are exploring mRNA technology for treating pancreatic cancer and cystic fibrosis, because it can deliver genetic instructions to correct or fight disease at the cellular level.

FUN FACT. Did you know that every cell in your body makes and uses mRNA? It’s true! mRNA is short for messenger RNA and every cell in your body makes and uses mRNA as the recipe or set of instructions to make all the proteins in your body. mRNA is not foreign or new. Our bodies have been making and using mRNA since the very beginning of human life!

Viral Vector Vaccines
Use a harmless, modified virus (vector) to deliver genetic instructions to your cells so they produce a target protein from the pathogen. That protein triggers immunity. An example: the Ebola vaccine (Ervebo), which uses a live but weakened viral vector.

Protein Subunit and Recombinant Vaccines
Contain purified pieces of the pathogen, like proteins, that train the immune system without using live components. An example is the Novavax COVID‑19 vaccine (Nuvaxovid), which uses recombinant proteins with an adjuvant to enhance the immune response.

Conjugate and Polysaccharide (Subunit) Vaccines
Use specific parts of bacteria, like the polysaccharide capsule, often linked (conjugated) to a carrier protein to enhance the immune response. Examples include Haemophilus influenzae type b (Hib), pneumococcal, and meningococcal conjugate vaccines.

Toxoid Vaccines
Contain inactivated toxins produced by bacteria, rather than the bacteria itself. They teach the immune system to neutralize the toxins. Examples include diphtheria and tetanus found in TDaP (tetanus, diphtheria and acellular pertussis) vaccine.

Vaccines Don’t Overwhelm Your Immune System

Some people worry that vaccines “overload” the immune system. The truth? Your immune system is built for diversity. Every B cell and T cell in your body has a unique specificity—it’s trained to recognize a different piece of a pathogen. Collectively, these cells offer tremendous diversity, capable of responding to millions of different threats.

Think of the immune system in your body like a hospital. There are many different types of specialists, such as cardiologists, pulmonologists, and neurologists, each trained for a specific field of medicine. If you come in with a heart problem, you’ll see the cardiologist (heart doctor), not the pulmonologist (lung doctor) or neurologist (brain doctor). Similarly, when a vaccine introduces a piece of a virus or bacteria, only the immune cells with the right “specialty” respond. The rest stay on standby waiting for the piece of pathogen they recognize.

Protection Without the Risk

After vaccination, your immune system has memory cells and antibodies ready to act. If you encounter the real pathogen, those memory cells recognize it instantly and mount a rapid defense, often before you even feel sick.

Vaccines don’t overwhelm your immune system. Vaccines guide immunity to make it smarter, faster, and better prepared.

FAQ About Vaccines

1. Can vaccines cause the disease they protect against?
No. Vaccines use inactivated pathogens, weakened forms, or just pieces of the pathogen (like proteins). They give your body a practice run to learn what the pathogen looks like to build defenses like memory immune cells and antibodies.

2. Why do we need additional doses (aka boosters) for some vaccines?
Over time, antibodies decrease and immune memory needs a nudge. Additional booster doses remind your immune system what the pathogen looks like, resulting in a refresher for immune memory cells and an increase in antibody production to keep your defenses strong.

3. Do vaccines weaken the immune system?
No. Vaccines actually strengthen – not weaken – your immune system. Vaccines train your immune system without overwhelming it. Your immune system is designed to handle thousands of challenges at once and vaccines guide it safely with harmless versions of a pathogen to build defenses.

4. Why do some vaccines protect for life while others need updates?
It depends on the pathogen and the formulation of the vaccine. Some viruses mutate quickly (like the influenza and SARS-CoV-2, the virus that causes COVID), so vaccines need annual updates. Other pathogens (like measles and polio) stay relatively stable, so one vaccine can last decades. Some formulations of vaccines, like live-attenuated, result in a robust immune response on their own while subunit and other formulations may require additional doses to keep protection at its peak.

5. Can my immune system handle multiple vaccines at once?
Yes! Your immune system encounters countless microbes every day. The number of antigens in vaccines is tiny compared to what it handles through every day life. Vaccines train your immune system without overwhelming it.

Want more information? Check out the trusted resources below!

Immunology Explained

https://immunologyexplained.aai.org/

Immunize.org

https://www.immunize.org/

Let’s Get Real

https://www.letsgetrealaboutvaccines.org/

Vaccine Information

https://www.vaccineinformation.org/

Healthy Children, The American Academy of Pediatrics https://www.healthychildren.org/English/Pages/default.aspx

The Vaccine Education Center, The Children’s Hospital of Philadelphia https://www.chop.edu/vaccine-education-center

Vaccinate Your Family

https://vaccinateyourfamily.org/

Voices for Vaccines

https://www.voicesforvaccines.org/

Immunize Colorado

https://www.immunizecolorado.org/

April English*, Aimee Pugh Bernard, Leigh Baxt, and Jess Steier

This article is in collaboration with Immunology Explained, an initiative by the American Association of Immunologists (AAI) to connect you to the science behind your health.

*This article is written through the lens of April English, an amazing and resilient person living with Scleroderma. The science elements were fact-checked and lightly edited for accuracy by Aimee and Leigh.

As a person living with Scleroderma (April), it’s hard to put into words what living with an autoimmune disease is like, let alone an invisible one. Most people picture someone with a chronic autoimmune disease as visibly unwell, perhaps disabled, or limited by their condition. But that’s not always the case. As the saying goes, never judge a book by its cover.

Scleroderma is an ‘invisible illness,’ which is an umbrella term for a medical condition that isn’t easily visible to others. Living with an invisible illness is challenging as it often involves judgment and criticism when others believe you look fine on the outside. I don’t [typically] look sick. To most people, on the outside, I might even seem like the image of a “healthy” adult - I’m involved in competitive sport, weightlifting, rock climbing, and I invest a lot in self-care and well-being.

But on the inside, my life looks a little different. I routinely ask myself questions others might never think about:

· Is that person coughing sitting across from me sick? Could that be the reason for my hospital visit?

· Will I eventually lose the ability to play the sports I love?

· Can I eat this, drink that, or will it cause acid reflux?

· Will my friends understand what I’m going through - or will they think I’m exaggerating?

· Is this symptom a progression of my existing condition, or something entirely new?

· Will my condition shorten my lifespan?

I also have a routine that most people in their 30s don’t:

· Checking my blood pressure

· Taking medications

· Tracking symptoms

· Regularly seeing multiple specialists and undergoing routine tests and procedures, such as blood work, biopsies, lung function tests, bone density scans, and ECGs.

· Trying to keep up with the latest research about my disease

This is my normal.

As for my body, I’m never quite sure what’s happening beneath the surface. Scleroderma is a progressive disease, and much of it only reveals itself when a new symptom appears, or an existing one quietly worsens.

And so, like many scleroderma patients, I’ve learned to live in the unknown.

When the Immune System Goes Wrong

Scleroderma is a chronic autoimmune disease of the immune system, blood vessels and connective tissue. An autoimmune condition develops when the immune system, which normally protects the body from harmful invaders, mistakenly attacks healthy cells and tissues. Scleroderma is a rare and complex autoimmune disease. It affects people in many different ways - everyone’s experience is different.

Scleroderma occurs when your body produces too much collagen, which is a strong, fibre-like protein that acts like scaffolding; it gives structure and support to your skin and connective tissues throughout the body. In scleroderma, the body produces too much collagen, causing it to build up where it shouldn’t. This excess can make the skin stiff, tight, thick, or scarred. In some people, the build-up also affects blood vessels, joints, muscles, and internal organs.

There are two main types of scleroderma: Localized and Systemic

Localized Scleroderma is a condition that affects only the skin. It causes one or more patches of skin to become hardened and thickened on different areas of the body. There are several types of localized scleroderma, and their severity can vary widely, ranging from mild, limited skin changes to more extensive areas of involvement.

Systemic Scleroderma affects internal organs, as well as the skin. There are two main types under the category of systemic scleroderma: limited and diffuse.

Limited cutaneous systemic sclerosis is a form of systemic sclerosis that typically develops gradually over time. It primarily affects certain areas of the skin, most commonly the hands and face, where individuals may develop telangiectasias, also known as broken or widened blood vessels. Although skin involvement is usually limited, internal organs can also be affected. The lungs are a particular concern, as some people may develop pulmonary hypertension, a condition characterized by high blood pressure in the blood vessels of the lungs.

Diffuse cutaneous systemic sclerosis is a form of systemic sclerosis that typically develops more rapidly than the limited cutaneous form. It often affects larger areas of the skin, leading to more widespread skin thickening and tightening. In addition to skin involvement, internal organs are commonly affected, particularly the heart and lungs. Because of its potential to impact multiple organ systems, diffuse cutaneous systemic sclerosis generally requires close medical monitoring and management.

Sine sclerosis is a rare form of systemic sclerosis in which there is little to no noticeable skin thickening or hardening. Despite the absence of significant skin involvement, the disease can still affect internal organs, such as the lungs, heart, gastrointestinal tract, or kidneys. Because it lacks the characteristic skin changes seen in other forms of scleroderma, sine sclerosis can be more difficult to recognize and diagnose.

What Scleroderma looks and feels like

For most people, scleroderma causes skin symptoms, such as patches of thick, hard skin that may become discoloured, itching, and tight skin that makes it harder to move your joints. Hard lumps of calcium may also deposit under the skin and tiny blood vessels (spider veins) or spots may appear just beneath your skin (telangiectasia). Painful sores may also form on fingers and toes (digital ulcers).

Localized scleroderma may develop gradually over months, or erupt more quickly over a period of a few weeks.

· Skin changes: itchy, burning, or sore. Thickened skin may become fixed and ‘stuck down’ across a joint such as the wrists, ankles, knees or elbows, restricting growth and mobility.

· Deep tissue involvement: deeper tissues on the face can lead to distortion of the natural facial contour and altered facial appearance. This may also result in fatigue, joint pain and muscle aches. Hair loss over the affected area may occur as well as headaches and more rarely, epilepsy. The eyes and teeth may occasionally also be affected.

Systemic Sclerosis often develops with Raynaud’s as the first symptom. It may come well before other symptoms - up to 10 years before. Other symptoms include:

· Skin changes: Skin can be itchy, tight and/or hardened, often around joints. Tiny calcium deposits can develop under the skin. Painful sores on fingers and toes (digital ulcers) may develop. Tiny blood vessels (spider veins) or spots appearing just beneath your skin (telangiectasia).

· Muscles: Poor functioning of the muscles in the upper and lower oesophagus can make swallowing difficult and allow stomach acids to back up into the oesophagus, leading to acid reflux, heartburn, inflammation and scarring of esophageal tissues.

· Organ involvement: Scarring or fibrosis occurring within the GI tract. Scarring or fibrosis may occur within the lungs. Heart involvement, for most, is often mild and very difficult to be sure whether it is present or not. For others heart involvement may be more severe. Like the heart, kidney involvement is variable and often mild. The eyes and teeth can occasionally be affected.

Piecing together a diagnosis

Many diagnosis journeys are a long and frustrating one. As you’ve learned, Scleroderma can take many different forms and affect different parts of the body, which can make it difficult to diagnose. It can take years to receive a proper diagnosis, often after new and/or progressed symptoms begin to develop. Some have experience of, sadly, not being taken seriously or being dismissed by healthcare professionals. And a delayed diagnosis can cause irreversible emotional and physical toll and damage.

Women make up 80% of scleroderma cases. My diagnosis of Systemic Scleroderma started with calling my general practitioner (GP) to express how my raynaud’s has worsened: even a short walk on a warm autumn day turned my fingers pale, cold and numb. Luckily, I was taken seriously by my GP, and was referred to a specialist right away - likely because I already had an pre-existing autoimmune disease - autoimmune hepatitis - and it’s common for people with autoimmune diseases to have more than one.

This took me down a path of visiting a new specialist - a rheumatologist, a physician specialized in diagnosing and treating conditions that affect the joints, bones, muscles and immune system. My rheumatologist analyzed additional blood work, checked physical symptoms (like pinching the skin), a skin biopsy, and even a test where the doctor looks at the bed of your fingernails through a microscope - called a nail fold capillaroscopy.

Systemic sclerosis can be difficult to diagnose as it often develops gradually. Many people live with unexplained symptoms for years before receiving a diagnosis. There is no single test or feature which gives a yes or no answer. Instead, the diagnosis is made after looking at the whole person, taking into account their symptoms, physical examination and clinical tests.

Combining several elements can lead to a diagnosis of Scleroderma and differentiate between Localized and Systemic Scleroderma.

· Blood tests for anti-nuclear antibody and biomarkers

· Blood pressure tests

· Skin biopsies

· Nailfold Capillaroscopy

· Imaging, including X-rays and CT scans

· Organ-specific testing for the heart (echocardiogram), GI tract (endoscopy), lungs (pulmonary function tests)

· Additional symptoms might include evaluation for gag reflux problems and Raynaud’s phenomenon

I’m incredibly fortunate in that my doctors believe the disease hasn’t progressed significantly. That’s why staying on top of symptom management is so important - it’s how we catch any early signs of change before anything becomes harder to address.

Living with that uncertainty can be scary at times. But I’ve also found it can be a powerful motivator. When my future feels unpredictable or uncertain, it drives me to achieve what I want to accomplish in my life, and serves as a fuel and reminder of what truly matters in life.

Treatments for Scleroderma

There is no cure for scleroderma and because scleroderma is complex, treatment can also be complex: treatment requires a team of different healthcare professionals.

The aim of treatment is to stop progression, shorten the duration of disease and avoid tissue damage. Treatment will be tailored to individual needs, depending on what type of scleroderma someone has and how it affects their body.

Treatments for Scleroderma include targeted treatments for the systems involved in the disease to manage symptoms.

· Skin. Topical treatments or creams can help with tightness or dryness of the skin. In severe cases immunosuppressants can help with these symptoms (mycophenolate, cyclophosphamide or methotrexate). In some cases intravenous immunoglobulin (IVIG) may also be used. UVA-1 phototherapy is also used at times.

· Raynaud’s Phenomenon. Blood pressure medications including calcium channel blockers (amlodipine or nifedipine), Angiotensin receptor blockers (losartan or valsartan), or Phisphodiesterase-5 (PDE-5) inhibitors (sidenafil or tadalafil) are used to dilate blood vessels and improve circulation which can prevent digital ulcers.

· Gastrointestinal Symptoms. Proton pump inhibitors can help manage severe heartburn and acid reflux (omerprazole, pantoprazole). If there are also intestinal motility issues, medications that ease bloating or constipation can also help (psyllium, loperamide, linaclotide).

· Lung complications. Immunosuppressants are often used if patients develop interstitial lung disease. Nintedanib was approved in 2019 to treat scleroderma-associated lung disease and works by inhibiting a combination of enzymes to slow lung fibrosis. Another medication approved in 2021, called tocilizumab, that inhibits a pro-inflammatory cytokine called IL-6 that reduces lung inflammation.

· Kidney complications. Kidney crises can be managed with blood pressure medications like ACE inhibitors (captopril).

· Pain & Joint Swelling. NSAIDs (non-steroidal anti-inflammatory drugs) are the first line treatment to manage these symptoms. Corticosteroids can also be used to relieve inflammation and pain.

· Non-medication treatments. Additional treatments may benefit patients with scleroderma including physical or occupational therapy to maintain joint mobility and muscle weakness. Treatments to manage effects of the disease may also include fat transfer or fillers or involvement of surgeons to treat joint contractures or limb asymmetry.

Emerging treatments

There are several new treatments in development for scleroderma.

· CAR T-cell therapy. An immunotherapy that involves removing a patient’s own T cells and reprogramming them to target a specific molecule on a cell of interest and infusing them back into the patient. While this is commonly done for patients with cancers of B cell origin, this type of personalized immunotherapy is now proving to be useful for some autoimmune diseases. For Scleroderma, a similar approach would be used to deplete the patient’s B cells for refractory disease. This may be more long-acting than some antibody-based immunotherapies such as rituximab.

· Targeted Biologics. Biologics that bind and block the interferon receptor, others that result in B-cell inhibition, and some that modulate T cells may be used. The combination of several agents aimed to modulate the immune system may work together with immune suppressants to provide improved effects.

· Anti-fibrotic medications. Bispecific antibodies or antibodies that have been fused together to target more than one specific molecule can target multiple pathways simultaneously, including those that drive fibrosis as well as those driving immune cell activation.

· Biomarkers. Research is continuing to focus efforts on discovering biomarkers that may be used for risk stratification and disease classification.

Final Thoughts

Living with autoimmune diseases has taught me that so much is still possible - even when it doesn’t feel that way.

The truth is, I’ve worked hard to get here. After my diagnosis, I made it my priority to understand my body more deeply - learning which treatments worked, which habits helped, and how to advocate for myself.

And as strange as it might sound, I have a lot to thank my diagnosis for.

Without it, I likely wouldn’t have become so focused on my health. I likely wouldn’t have pursued a career in health promotion, a role in patient and public involvement, or found my way into science communication. I likely wouldn’t have found my lifelong partner or discovered who my true friends are - the ones who show up, no matter what.

And I truly don’t think I’d be who I am today. Driven, empathetic, passionate, with a zest for life. Someone who gets to hear from others that I’ve inspired them to advocate for their own health.

My diagnosis is often my fuel. And for that, I’m grateful.

I don’t think a diagnosis should define us. So I decided, from the very start, that it wouldn’t define me.

-April English

Resources for Scleroderma Support:

Scleroderma and Raynaud’s UK

Project Scleroderma

National Scleroderma Foundation

Scleroderma Research Foundation

The Scleroderma Education Project

Scleroderma Education Library

It was 3 a.m. on a Tuesday when my (Sarah) phone rang while I was on call. On the other end was a first-time mom in her second trimester, breathless with worry before she even finished saying hello.

She’d spent the weekend helping her sister, whose three-year-old had a cough. I never get sick, she told me, so she hadn’t thought much of it at the time. But now she had a cough of her own and a fever hovering at 101. Her obstetrician had given her a list of medications considered safe in pregnancy. Acetaminophen was on it. And yet she hadn’t taken it.

She’d read online that Tylenol (acetaminophen) could be bad for her baby. She didn’t want to do the wrong thing. So she worried through the day, worried through the night, and finally, after hours of fretting, called the office. And there we were, in the quiet of early morning, talking about fever and acetaminophen in pregnancy.

This wasn’t a one-off experience, either on call or in the office. But it stayed with me because of how much stress she carried into that call—and how clearly it was rooted in care. All she wanted was to do the right thing for her pregnancy.

What she was carrying that night was a contradiction we hand pregnant women all the time. We tell them their bodies are doing something powerful and miraculous, and in the next breath we tell them their immune system has gone soft and needs protecting. We talk about pregnancy as powerful and its immune system as fragile. Both ideas can’t be true at the same time, right?

So what is actually happening to the body and immune system during pregnancy? And why does the idea of immune weakness persist, even when biology tells a far more remarkable story? Pregnancy isn’t a failure of the immune system; it’s one of the most sophisticated examples of what the human body can do.

Reframing Pregnancy as a Physiologic Adaptation with Immune Recalibration

When I (Aimee) teach first-year medical students about pregnancy and the immune system, I ask them to explain a massive biological paradox: how does an immune system designed solely to seek and destroy invaders tolerate a “guest” that is fifty percent foreign for nine whole months? The developing fetus carries the other parent’s DNA, meaning it’s essentially an unmatched transplant. By all accounts, the body’s defenses should reject it instantly. But instead of attacking, the maternal immune system shifts gears to tolerate and protect it. Someone always asks how that is even possible, and that question is the whole subject. The pregnant body isn’t weakened, it’s recalibrated. This is especially true of the immune system.

The immune system is strategically adjusted to allow a genetically distinct non-self (half‑foreign) fetus to grow within the body while still defending the pregnant parent - and developing fetus - from infection. Some immune responses are intentionally dialed down, such as certain T‑cell–mediated responses that normally attack foreign cells become less aggressive, and inflammatory pathways that could threaten the developing placenta are kept in check. None of this is the immune system stepping back. It is the immune system doing something more challenging - to decide what to tolerate and what to fight.

Physiology Meets Immunology: Pregnancy Requires Precise Coordination

Pregnancy transforms nearly every major body system. The cardiovascular system increases its blood volume dramatically, the respiratory system adapts to bring in more oxygen, and metabolism rewires itself to fuel both parent and baby. And then there’s the placenta, an entirely new, temporary organ that anchors the pregnancy, delivers nutrients, removes waste, and communicates constantly with the immune system. It’s important to distinguish the placenta from the uterus: the uterus is the pregnant parent’s own organ, while the placenta is composed of fetal tissue that embeds within the uterus. That distinction matters, because the immune system must recognize the placenta as genetically distinct (aka ‘foreign’) yet avoid attacking it. These coordinated physiologic changes highlight how pregnancy relies on immune cooperation and adaptation, not immune shutdown.

To support a developing fetus, the immune system adopts a finely tuned balance between protection and tolerance. Some of these changes happen locally, right at the maternal–fetal interface, where specialized immune cells help the placenta grow and prevent harmful inflammation. Uterine natural killer (uNK) cells, for example, are not the aggressive infection‑fighters we typically associate with NK cells. NK cells elsewhere in the body detect and destroy ‘altered self’ cells. They are known to hunt down altered self cells that are virus-infected or cancerous and destroy them. You would expect a population of killers to be the last thing you want crowding around a half-foreign organ. Instead they show up to the maternal-fetal interface in pregnancy and take on a nurturing role, helping remodel blood vessels so the placenta can deliver oxygen and nutrients to the fetus. Another key player is the population of regulatory T cells (T‑regs), which expand during pregnancy to promote tolerance and keep maternal T cells from mistakenly targeting fetal tissues. Meanwhile, systemic immunity remains active, allowing the pregnant parent to respond to infections. This state is best understood as immune tolerance, not immune failure: the body is deliberately learning to live with something partly foreign while keeping its defense system online.

Maternal Vaccines Power Immune Protection

One of the most remarkable outcomes of this immune partnership is the transfer of protective antibodies across the placenta in later pregnancy, giving newborns their first immune shield after birth, a process that becomes even more powerful when the pregnant person receives the recommended maternal vaccines. Vaccination during pregnancy against influenza, COVID‑19, RSV, and pertussis (through the TDaP vaccine) prompts the maternal immune system to generate high‑quality, antigen‑specific antibodies that readily cross the placenta and protect babies during their most vulnerable early months. These vaccines are strongly recommended by leading medical organizations because they reduce severe disease in the pregnant person and provide essential passive immunity to the newborn. For example, ACOG emphasizes that maternal immunization, particularly for influenza, COVID‑19, and RSV, prevents severe respiratory illness and improves neonatal outcomes, while TDaP during pregnancy is crucial to protect newborns from pertussis before they can be vaccinated themselves.

By intentionally stimulating the immune system during pregnancy, these vaccines work with the body’s built-in immune defenses to provide protection. Pregnancy isn’t an immunologic weakness; it’s an elegant reorganization of local and systemic immune components that support both parent and baby, and maternal vaccination leverages that system to provide life‑saving protection during pregnancy and the first several months of life of the newborn after birth.

What Actually Supports the Immune System in Pregnancy

Vaccination, Nutrition and Sleep! Oh My!

Supporting immunity in pregnancy isn’t about trying to bolster something deficient; it’s about providing what an exquisitely tuned biological program needs to operate. In practice that comes down to three things we tend to underestimate: vaccination, nutrition, and sleep.

Vaccination

One of the clearest examples is vaccination. Contrary to the myth that pregnancy blunts immune responses, pregnant people consistently generate robust antibody responses to recommended vaccines: including influenza, COVID-19, RSV, Tdap, and Hepatitis B. Those antibodies don’t just protect the pregnant person. They cross the placenta and enter fetal circulation, conferring passive immunity to the infant after birth, often for months, during the window before a baby can be vaccinated themselves. The non-live vaccines we recommend during pregnancy are safe and effective precisely because they engage an immune system that can respond and should be recruited to protect both mother and baby.

Nutrition

Nutrition plays a similarly foundational role. Plasma volume increases by more than 40 percent during pregnancy, which drives a dramatically increased demand for iron to maintain oxygen delivery. Inadequate iron undermines both oxygen transport and the capacity of immune cells to do their work. Folic acid supports DNA synthesis and cell division throughout the body, including in immune cells. Calcium, magnesium, zinc, vitamin D, and iodine all matter too.

Nutrients from food tend to be better absorbed and used than the same nutrients taken in isolation, in part because they arrive together, in the proportions and chemical forms the body is built to handle, alongside fiber and other compounds that shape how they’re processed. Prenatal vitamins and a small number of targeted supplements fill specific, well-documented gaps, folate and iron chief among them. But more is not better, and the instinct to take everything just in case is worth resisting. Many supplements are unnecessary in pregnancy, and some carry real risk, in part because the FDA does not review supplements for safety or effectiveness before they reach the market. A manufacturer sets the dose, makes the product, and sells it; the agency generally steps in only afterward, once a product already on the shelf turns out to be contaminated or mislabeled. That regulatory gap is exactly why the supplement aisle is the wrong place to improvise. Your OB-GYN can tell you which supplements you actually need and which to skip.

Sleep

Sleep and stress are often framed as lifestyle variables. Biologically, they are core regulators of immune function. During sleep, particularly slow-wave sleep, the immune system shifts toward processes that support long-term defense: regulating inflammation, consolidating immune memory, coordinating the signals that keep adaptive immunity sharp. Disrupted sleep pulls the system toward a more pro-inflammatory state and weakens immune responsiveness, effects that have been documented in reduced antibody responses to vaccines even in otherwise healthy adults.

Chronic stress operates through similar pathways. Sustained activation of stress responses leads to prolonged cortisol exposure, which dysregulates immune signaling and pushes cytokine profiles toward persistent inflammation. Sleep disruption and chronic stress do not simply weaken the immune system. They distort it, pulling it away from the finely tuned adaptations pregnancy requires. Seen this way, prioritizing sleep and managing stress aren’t peripheral wellness advice. They are integral to pregnancy care.

What Disrupts an Already Calibrated System

Many of the things that disrupt immune function during pregnancy are not exotic or mysterious. They are constraints on a system already operating at high demand.

Nutrient deficiencies are a clear example. Immune responses depend on rapid cell division, protein synthesis, and tightly regulated signaling, all of which require adequate micronutrients. During pregnancy, those demands increase alongside expanded blood volume, placental growth, and fetal development. When iron or folate is insufficient, the immune system isn’t weakened so much as under-resourced, creating bottlenecks in processes that would otherwise run smoothly. That effect can extend to the newborn, because nutritional deficiencies in utero can impair the baby’s immune response after birth.

Chronic stress and poor sleep work the same way, quietly and cumulatively, nudging the system toward persistent inflammation instead of the balance pregnancy depends on. The effect is easy to miss precisely because it is gradual, which is part of why it gets dismissed as something a pregnant person should simply tough out.

Underlying medical conditions add complexity. Autoimmune diseases, metabolic disorders, and the medications used to manage them all shape baseline immune activity. These factors don’t negate immune adaptation, but they change its starting point and deserve individualized attention.

Fever is perhaps the most misunderstood disruptor of all. It is a normal physiologic response to infection. But in pregnancy, sustained fever carries real risks, particularly during sensitive windows of fetal development. So treating fever while pregnant is important. Ibuprofen is contraindicated in pregnancy, leaving acetaminophen as the primary option. Treating fever with acetaminophen is not about suppressing the immune system or increasing long term diagnosis in the fetus. It is about responding to a physiologic signal in a context where unchecked fever is itself the danger. The data support this clearly: managing fever is part of protecting both maternal and fetal health. This is what I (Sarah) found myself explaining at 3 a.m. to the mom with the 101 fever. She had a safe medication sitting in her cabinet and a fever doing real harm, and she had talked herself into the more dangerous of the two options because a headline told her the safe one wasn’t safe. I (Sarah) told her to take the acetaminophen. Then I stayed on the line a while longer, because the fever was never really the thing keeping her up. The fear was.

Pulling the Threads Together: Adaptation, Not Fragility

The factors that disrupt immune balance in pregnancy don’t point to a system that is fragile. They point to one that is responsive, context-dependent, and worthy of thoughtful care.

Pregnancy asks the body to do something rare in human biology: to undergo sweeping physiologic change while maintaining immune vigilance and restraint at the same time. Blood volume expands, metabolism shifts, and a temporary organ (placenta) forms to support a developing fetus. In response, the immune system adapts: locally recalibrating tolerance, systemically maintaining defense, and coordinating signals across multiple organ systems. These changes are not competing processes; they are integrated ones. The body changes, the immune system responds, and together they protect pregnancy.

This coordination is not new or experimental. It reflects a system shaped and refined over evolutionary time, one that has been tested across countless pregnancies long before modern medicine began to observe it. That does not mean pregnancy is without risk, or that medical care is unnecessary. It means that the baseline state of pregnancy is not one of breakdown, but of design: complex, responsive, and resilient when supported appropriately.

Final Thoughts

When confusion arises, it is rarely because pregnancy biology is inherently fragile. More often, it is because incomplete or distorted information gets layered onto a system that is already doing something demanding. Advice meant to “avoid harm” can inadvertently create fear. The result is not better protection, but more anxiety. Like the 3 a.m. conversations that grow out of uncertainty about what is truly safest to do. This is the same misunderstanding that turns pregnancy-recommended vaccines, designed to engage a responsive immune system and extend protection to the newborn, into sources of doubt rather than reassurance.

Pregnancy is one of the most sophisticated physiological challenges the immune system successfully accomplishes.

Understanding pregnancy as adaptation rather than weakness changes the frame entirely. It allows us to see evidence-based supportive care not as interference, but as partnership with biology.

The immune system doesn't retreat during pregnancy — it adapts, negotiates, and rises to the occasion. That's not a vulnerability to manage. That's a triumph worth marveling at.

Stay curious!

One of the reasons behind this communication gap is that scientists spend years learning how to communicate with other scientists but rarely or, in most cases, never trained to explain our work to a neighbor, a parent, or the person sitting next to us on a plane. Suddenly, all of our usual communication tools stop working.

Effective science communication begins when we stop focusing on what we want to say and start thinking about what our audience needs to hear.

As a PhD immunologist and medical educator, I’ve seen firsthand how difficult and important it is to communicate science clearly. Whether I’m teaching future health professionals, talking with members of the public, or developing science communication resources, I’ve learned that expertise alone isn’t enough. Effective communication starts with understanding your audience and finding ways to connect new ideas to what they already know and care about.

Scientists are trained to communicate with precision, accuracy, and efficiency using technical language (aka ‘jargon’) specific to our fields. We’re rarely trained to adapt our science (and technical language) into easy-to-understand, clear language that resonates across a variety of audiences. As a result, our messages don’t always land the way we intend.

I’ve seen this challenge repeatedly throughout my career. And it’s not because scientists aren’t good communicators, but because we’re communicating exactly the way we were trained. The problem is that the same explanation that works for a colleague at a conference is unlikely to work for a patient, a policymaker, a journalist, or a curious neighbor.

The key is to start with your audience and adjust your explanation accordingly.

To help trainees develop this skill, I created a practical five-tier framework that helps scientists translate their work for different audiences without sacrificing accuracy or meaning. I originally developed this approach years ago while mentoring graduate and medical students who were struggling to explain their research beyond the classroom or laboratory. Since then, I’ve found it to be a useful tool for anyone looking to communicate science more clearly and effectively.

Why We Need a Multi-Tiered Approach

One of the biggest challenges in science communication is that there’s no single version of an explanation that works for every audience. The way I would explain the immune system to a colleague, a medical student, a journalist, or a middle school student would look very different.

I’ve noticed that scientists often struggle at either end of the spectrum. Sometimes we lean too heavily on technical language because that’s how we’ve been trained to think and communicate. Other times, in an effort to make our work accessible, we simplify so much that we strip away important context, nuance, or uncertainty.

Effective science communication isn’t about making science simpler for the sake of simplicity. It’s about making it understandable and relevant for a specific audience while preserving the integrity of the science. I like to think of science communication as a process of translation rather than simplification. With each step, you’re challenged to identify what is truly essential, refine your language, and connect your message to what your audience already knows and cares about. The goal is to meet people where they are without losing the accuracy, meaning, or the wonder of the science itself. This is a much more challenging task than it sounds.

One of the most common mistakes in science communication is swinging too far in either direction: some scientists overwhelm their audience with dense, jargon-heavy explanations that can feel exclusionary or elitist, while others overcorrect by simplifying so much that their message comes across as condescending. Yikes! Neither of these outcomes allow the audience to feel connected to our science.

The real skill lies in finding the balance between these extremes, and that balance depends entirely on your audience. A useful way to think about this is as a process of progressive translation through a multi-tiered approach. With each step, you are forced to clarify your own thinking, identify what truly matters, and adjust your language without losing the core intent of the message. The goal is not simplification for its own sake, but alignment and meeting your audience where they are while doing your best to maintain the integrity and nuance of the science.

Let me introduce my 5-tier framework for translating your science to fit your audience…

» The 5-Tier Framework

Tier 1. Colleagues in Your Field

Explaining your work to a colleague the way you’ve been trained to communicate in your discipline.

• Full use of jargon and technical terminology (unrestrained!)

• Assumes shared background knowledge

• Prioritizes precision and specificity

I always recommend starting with this tier as it is your source material. After years of training in your field of expertise this tier comes most naturally. The use of technical language or jargon has a purpose: it’s precise and efficient but it’s only effective for a very small audience – the people in your field and area of expertise – and needs further translation for other audiences.

Tier 2. Cross-Disciplinary Scientists

Explaining your work to a scientist in a different field.

• Some technical terms remain, but require brief explanations

• Adds context and scaffolding

• Reduces assumptions about shared knowledge

I recommend moving to Tier 2 as the next step in translation. Here you translate your science without fully simplifying but do need to add a bit of context and unpack some of the science.

Tier 3. Science-Curious Public

Explaining your work to people who are curious about science. A good point of reference here might be people who read Scientific American or the science section of a newspaper.

• Minimal jargon

• Clear explanations of core concepts

• Focus on why it matters – meaning and impact

I recommend moving to Tier 3 as the next step in translation. Shift is to focus less on methods and how you arrived at your scientific findings. At this level, focus more on meaning and impact. People care less about how you did it and more about what it tells us. Focus on how your science solves a problem or fills a gap in knowledge and, most importantly, how it impacts the world around us.

Tier 4. General Public

Explaining your work to people with no assumed science background. A good point of reference may be a family member or friend who you know does not have a background in science. Keeping in mind someone you have a relationship with as you translate for this tier can be helpful as you can cater the conversation (in your head or on paper) to this person you have in mind.

• Clear, everyday language

• Big-picture framing

• The use of sci comm tools, such as analogies and metaphors, can be useful here

• Emphasis on relevance and clarity

I recommend moving to Tier 4 as the next step in translation. Shift is to focus on understanding and connection. At this level, focus on the relevance of your science to the world outside of the laboratory as well as making connections that inspire understanding. Making connections (to the person and to the science) is where trust in science is built.

Tier 5. Young Audience (aka ‘Future Scientists’)

Finally, you’re translating your work for children – our future scientists!

• Highly simplified ideas

• Imaginative framing

• Energy, curiosity, and excitement

I recommend moving to Tier 5 as the final step in translation, even if you don’t intend to explain your work to a classroom full of 5th graders (see screenshot below). At this level, you are no longer just explaining your science - you are inspiring the next generation!

What This Looks Like in Practice

Let’s take a single concept and move it through all five tiers.

Prompt. How mRNA works inside a cell

Tier 1. Colleagues in Your Field

mRNA is transcribed from DNA in the nucleus and exported to the cytoplasm, where it serves as a template for translation by ribosomes. Codon–anticodon pairing with tRNA facilitates the sequential addition of amino acids to form a polypeptide chain. Post-translational processing then determines the protein’s final structure and function.

Tier 2. Cross-Disciplinary Scientists

mRNA carries genetic instructions copied from DNA and moves from the nucleus to the cytoplasm. There, ribosomes read the mRNA sequence in sets of three bases and, with help from tRNAs, assemble amino acids into a protein. The protein then may undergo further processing and fold into its functional form.

Tier 3. Science-Curious Public

Inside cells, messenger RNA (aka ‘mRNA’) acts like a temporary set of instructions copied from DNA within the nucleus or center of the cell. From there, the mRNA travels out of the nucleus and finds a ribosome, which reads the instructions and builds a protein piece by piece using building blocks called amino acids. These proteins are then used by the cell to keep the cell functioning.

Tier 4. General Public

Inside every cell in our body is a ‘messenger’ that we call messenger RNA, or mRNA for short. mRNA is like a recipe copied from the cookbook of DNA, that contains the genetic instructions for everything our body needs to function. mRNA recipes are only copied from the DNA cookbook when they are needed. Machinery in our cells, called ribosomes, read the mRNA message and use it to build proteins. One example of a protein we need to make every day is insulin. Insulin breaks down sugar from the food we eat into energy.

Tier 5. Young Audience (aka ‘Future Scientists’)

DNA is the cookbook that contains all the instructions for life. We have a DNA cookbook in every cell inside our bodies – heart cells, lung cells, skin cells, brain cells – all the cells! mRNA is like a recipe card inside your cells for tiny machines called proteins that help our cells stay alive and working. To make proteins, the cells in our body follow the mRNA recipe step by step until it’s done and the protein is made. A fun fact about mRNA is that after the cell uses the recipe card to make all the protein it needs for the task at hand, the mRNA recipe card gets thrown away! If that protein is needed again later on, the cell copies off a new mRNA recipe card from the DNA cookbook.

How to Use This Framework

Here’s a simple way to apply this to your own work:

1. Start at Tier 1

Write your explanation as you normally would for your field.

2. Translate tier-by-tier

Move down one tier at a time and don’t skip any tiers. Each level forces you to rethink and distill your message.

3. Identify what changes

• What terms did you remove or define?

• What details did you keep or discard?

• Did your emphasis shift from mechanism to meaning and/or impact?

4. Practice regularly

Take one sentence from your current work and rewrite it across all five tiers. I encourage my mentees to do this with convoluted titles from journal articles.

The more you practice, the faster and easier this process becomes. If you do this often enough, you will easily be able to slide from one tier to the next without much difficulty. incredibly powerful.

Common Challenges and Ways to Reframe Your Thinking

“I don’t want to oversimplify my work.”
You’re not removing accuracy, you’re changing emphasis.

“I don’t know how to make my science accessible.”
Accessibility isn’t a natural talent that you are either born with or not, it’s a skill built over time through iteration and trial-and-error.

“This takes too long.”
This process actually saves time by clarifying your thinking for talks, grants, funding pitches, teaching, and writing. All the things we scientists do and care about in our profession.

Call to Action! Try It Yourself

Pick one concept from your current research and run it through all five tiers. You may be surprised at what you discover - not just about how to explain your work, but about how well you understand it yourself.

The best science communicators aren’t simpler thinkers. They’re better translators.

The cost of this is not abstract. Even after a decade or more of training, most scientists were never taught to explain their work to anyone outside their field, and the result is public confusion, eroding trust, and discoveries that never translate into real-world impact. At the other end, a generation encounters science for the first time with limited exposure and few real-life role models to help them see themselves within it.

Science deserves to be shared with everyone, at every age. That means training the scientists and healthcare professionals at one end, and not forgetting the youngest audience at the other.

Nurturing Wonder: Introducing Science in Early Childhood

I, Leah, am a cell biologist by training, and for much of my PhD and postdoc I sat in dark rooms at a microscope, looking at cells. I found them fascinating, and beautiful, and I kept wanting to show the people around me what I was actually doing all day. So I started illustrating the cells I was seeing, and that turned into a whole career in visual science communication, away from the bench and into design.

Becoming a parent changed my audience. I wanted to share cell biology with my toddler, and realized there was not much out there to do it with. There are shelves of books about tractors, dinosaurs and farm animals, yet barely anything about the world we are actually made of. So I started Lupe - a free library of printable science for babies and toddlers.

I show my daughter cells the same way I show her animals and cars - not to teach her biology, but I would love for a cell to become one of the ordinary things in a child’s world, no stranger than a car or a dog. At this age it is not going to be about comprehension, but about familiarity. We don’t usually teach biology until high school, and by then it can already feel like something that is not for them, something reserved for clever people. I want that familiarity to be there long before that idea has a chance to set in, and to enter a child’s world during the window when they are most open to curiosity and wonder.

The first person who talks to a kid about science is almost always a parent, and most parents aren’t scientists, many of them lack confidence about it. So half of what Lupe is really doing is giving the parents the words and the material to have the conversation at all.

Every pack also has a high-contrast black-and-white set, made for newborns, who see bold contrast before they can focus on color.

With Lupe, I design all my illustrations to keep them from looking like education - no arrows or labels, nothing that reads like a textbook, nothing clinical or scary. I adapt the language so a small child or a non-scientist can follow it, but I still call things what they are: I don’t say “food slide,” I say “esophagus.” I don’t think esophagus is any harder for a two year old than helicopter, they are both just long words for a real thing. A child who can say dinosaur, or even tyrannosaurus, can say esophagus too.

If we make the words ordinary early, and put them in the parent’s hands instead of waiting for the classroom, science is not something a child encounters for the first time in school, but part of the background of their world from the start.

But making science familiar in those first years only opens the door. Keeping it open takes people trained to talk about their work all the way up the chain, and that is the part of the system we have neglected for just as long.

Beyond the Bench: Embedding Communication in Scientific Training

I, Aimee, spent 16 years becoming a scientist and in all that time, not a single minute of my required training was devoted to learning how to communicate my work to the people outside of the walls of academia or paywalls of scientific journals.

Ironically, my own entry point into science communication didn’t come through formal training at all. It started at home. When my twins were young, I found myself wanting to explain what I did as an immunologist in ways they could understand. I simplified, translated, and reimagined complex ideas into stories and visuals. By age 10, my daughter produced a strikingly accurate drawing of an immune response (below). She depicted immune cells interacting with bacteria, signals firing, and defenses mobilizing. It was clear evidence that when scientific ideas are embedded early and communicated thoughtfully, people of any age can grasp even complex biological systems.

Since earning my PhD in 2001, I’ve learned that the absence of communication training weakens the very ecosystem that science depends on to move forward. A lack of public understanding and trust carries institutional and societal costs. Funding priorities often depend on public and political support, yet the people responsible for advancing knowledge are rarely equipped to advocate for it in ways that resonate beyond academic audiences. Scientific innovation may be stalled because its meaning and relevance are not accessible.

This gap is most visible at the top of the training pipeline, among established researchers who are experts in their fields but have limited experience with public dialogue. This raises a more fundamental question: where should this skill have developed? If scientists reach the end of their formal training without learning to communicate broadly, the issue is not a late-stage omission but a systemic one.

One possibility is that science communication should be integrated much earlier in professional training: during undergraduate education, in graduate programs, or even as part of laboratory culture itself. Embedding communication as a core scientific competency (rather than an optional add-on) would signal that explaining one’s work is not separate from doing it.

Another possibility reaches further back still. If curiosity, storytelling, and audience awareness were cultivated from early education onward, future scientists might never see communication as an external demand, but as an intrinsic part of how knowledge is created and shared.

Ultimately, the question is not simply when scientists should learn to communicate, but why the system has long treated this skill as unnecessary. Addressing that question invites a reimagining when and where communication skills should be embedded within the training pathway so that the ability to connect science to society is part of its core and developed from the very beginning.

From Insight to Action…

Science communication across the lifespan does two things at once: it protects curiosity at the start of a life and rebuilds trust at the height of a career.

If you’re a parent or caregiver of a young child, you don’t need a science background to begin. Start now, in the ordinary, everyday moments, and use whatever helps, Lupe’s printable science library is free for exactly this. Make the words familiar early, and you give a child the sense that science was theirs all along.

And if you’re an academic leader or a scientist in training, it’s time to treat communication as a core scientific skill rather than an optional extra, and to build it into curricula and professional expectations. Our work isn’t finished when we’ve shared it with colleagues, at conferences, and behind the paywalls of journals. It’s finished when we’ve made it understandable to the people it’s meant to serve. That is how we rebuild trust in science, and there has never been a more important time to do it.

Two ends of one life, and the same simple commitment: talk about science with the people in front of you, in language they can actually understand.

While writing my talk, I crafted it like a play, treating each section of my message as its own scene. This approach was especially useful for flow. Like in a play, each scene needed to have its own message but also transition naturally into the next, building the storyline and guiding the audience from one idea to another coming together into one powerful and integrated story. Instead of wrestling with one long script, I focused on shaping distinct ideas (scenes) that contributed to the entire story. This approach also pushed me to think visually, to imagine the image that would be created for each scene to allow the audience to hear and see each part of the story.

I also selected this ‘scene-by-scene’ approach to help me memorize the entire 15-minute talk. If you’ve never given a TEDx talk, it’s important to know that all TED talks are memorized. There is no teleprompter, no notes, and no talking points coming through the headset. If you forget your lines, the talk won’t happen. This was the only element that gave me pause when accepting the invitation to speak. I was petrified (as a mid-career scientist who hasn’t had to memorize anything for years!) that I wasn’t going to be able to memorize my talk.

Looking back, I’m thankful I ventured into uncomfortable territory and am thrilled to report that I remembered the vast majority of the talk. However, immediately after I finished my talk, I realized I did forget a key point (that I’ve flagged below) but I’ve accepted it and realize that delivering 99% of my message is much better than zero. I am incredibly grateful for the opportunity offered to me by the TEDxCU selection committee. Special shout out to Michael Burns, Assistant Teaching Professor in the College of Communication, Media, Design, and Information at CU Boulder, and the lead of the TEDxCU team.

I invite you to sit back, relax, and read the talk itself below, presented as a series of scenes with distinct visuals so you can experience it the same way I built it, one intentional scene at a time that combined tell a story that communication training is essential to science and medical education…

Opening Scene. The Science ‘Swear’ Jar

You see this jar? It’s a swear jar - but it’s not your typical swear jar. Most people get swear jars because they swear or use curse words. My jar is different - it’s a science swear jar. My daughter made it for me when she was 10 years old. The rule is simple: every time I talk about science when no one asks me to, I have to pay the jar.

As you can see, it’s full - and this isn’t the first time. Over the last several years, it’s been emptied and filled many times! It turns out that I have an exceptional ability - although some would say annoying ability - to insert science into any conversation.

Act 1. Introductions

Let me tell you a little bit about who I am - the person who pays the jar. I have 3 professional roles: I’m an immunologist, an educator and a science communicator.

In my first role I’m an immunologist, a scientist who studies the immune system, the body’s built-in mobile defense against infection. I fell in love with immunology in college. Listening to my professor describe the complexity and elegance of the immune system was mind-blowing! I was hooked! And I’ve devoted my life to immunology ever since!

And I’m incredibly lucky because in my second role as an Associate Professor at CU Anschutz, I am the immunology content director for the CU School of Medicine, and I have the privilege and honor of teaching immunology every day :) Teaching and being a teacher is the heart and soul of who I am. Teaching was the motivation behind my pursuit of a PhD and my career in science.

Sharing my knowledge and enthusiasm for science fills me with joy! and brings me to my third role as a science communicator. For the past 25 years, science communication has been my passion project - a labor of love I’ve pursued in every spare moment of time. I’ve written blogs, op-eds, and guest commentaries. I’ve given talks in bookstores, at science clubs, and in coffee shops. I’ve recorded dozens podcasts and shared hundreds of posts across social media. If there’s a way to share science, I’ve tried it!

Act 2. Setting the Stage for ‘On the Contrary’

Here’s the challenge: most scientists are like me. We live, eat, and breathe our science and want to share it with everyone we meet

And here’s the catch: we were never taught how to translate our science into plain language, and our explanations don’t always land the way we intend. Scientists like me spend years in training to learn to be a scientist but none of our training includes science communication.

Act 3. My Journey into Science (a typical PhD path)

Let me describe my journey into science for you…

It all started with a 4-year bachelor’s degree in biology. Followed by 2 years in a biochemistry lab after college to gain experience in the real world. Followed by 5 years (actually 4.5 years but I didn’t want to brag onstage) of graduate school to get my PhD. And another 5 years in 2 different postdoctoral positions to gain even more lab experience.

That’s 16 years of training where every step of the way I was rewarded for learning and using the technical language or jargon of science.

You see, scientists in training are viewed as “promising” by experienced scientists if we learn the technical language or jargon of our fields as fast as we can so we can fully participate in the science around us - by listening to and understanding seminars, communicating with peers and faculty, and engaging with the scientific community.

During training, we’re so focused on fitting in and becoming scientists ourselves that we don’t think about how we sound to the people outside of our science labs and lecture halls.

Act 4. Compare and contrast jargon and accessible language

Let me give you an example of what years of practice using science jargon sounds like…

Vaccines work by introducing an antigenic stimulus that primes the adaptive immune system, facilitating the selection, activation and clonal expansion of antigen-specific lymphocytes. This establishes the generation of high-affinity neutralizing antibodies and the development of robust immunological memory, which results in long-term protection upon subsequent pathogen exposure.

Raise your hand if you want to hear it again without the jargon?

Vaccines work by introducing a harmless version or piece of a virus into your body to give your immune system something to train on to practice fighting the virus and build immune protection.

Let me describe this to you in the context of the annual flu vaccine. The flu virus is basically a circle covered in little spikey proteins all around the outer surface.To make the flu vaccine, all of the little spikey proteins are cut off - it’s like the virus is getting a haircut - and those chopped off bits are used to make the vaccine. The rest of the virus - that whole inner circle which contains the virus’s genetic material - is thrown away and not used! After a vaccine, your immune system is trained, like a martial artist, to recognize and fight the virus “out in the wild” - at the grocery store, the gym or a TED talk - your immune system is prepared to fight!

Act 5. Science communication is not rewarded

Over the years, I’ve realized we scientists aren’t always as prepared as our immune system, especially when it comes to communicating what we do and why it matters. Since earning my PhD in 2001, I’ve reflected on my own journey and noticed all the barriers we scientists face to engage in science communication. I know firsthand because I’ve had to overcome these barriers to get to where I am today.

Let me explain what I mean through the lens of promotion…

Like everyone else, scientists have criteria we must meet to keep our jobs and be promoted. Communicating our science to the public - beyond the walls of academia and the paywalls of scientific journals - is not a part of those criteria. At most universities, science communication experience is not even listed as something that could help you get promoted or hired.

Why is this? Like any promotion system, scientists are expected to show progress through generating data, publishing papers, and securing funding - and all of this progress happens in the laboratory. Unfortunately, connecting with the community pulls us out of the lab where our value and progress are measured. We’re trapped in a system where leaving the lab and connecting with the community slows our progress.

Act 6. The Paradox of Science Communication

And that’s the paradox: we scientists desperately want to share our work, but we’re not supported or trained how to do it. In a strange twist of fate, the systems designed to advance scientific knowledge for humanity have isolated it from the public eye. The problem isn’t a lack of willingness – on the contrary – it’s a lack of training and support.

Act 7. The Impact of Miscommunication

So why does this matter? Why should scientists learn to communicate their science to the public? Let’s all think back to COVID as an example of why science communication is so incredibly important. Remember the confusion? The virus was new and spreading quickly, mask guidelines changed, and vaccines were misunderstood.

While scientists were scrambling to learn about the virus and explain the science, misinformation was spreading like wildfire wrapped in language that was simple and easy to understand and easy to share. And the headlines kept screaming: “Scientists keep changing their minds!”

But here’s the truth that no one explained to the world: science changing its minds isn’t a weakness - it’s the very strength of science. Changing our minds is a superpower that allows us to be adaptable, flexible, and respond to new information. Let me flip the script. Science changes not because it’s broken… but because the process works. Every new piece of evidence sharpens our understanding and brings us closer to the truth.

Act 8. The Impact of Misinformation

Now let me ground that in something you do every day - think about your GPS.
You’re driving, everything’s fine… and suddenly there’s a crash up ahead.
What happens? Your GPS instantly reroutes you. You don’t throw your phone out the window. You do not accuse it of lying to you. You trust the update because it’s based on new data.

Science works the same way. Adaptability isn’t a flaw. It’s a feature.

But when we don’t communicate why things are changing, people get frustrated and confused and become mistrustful. I get it. Right now, misinformation is winning the communication game. Not because it’s right. But because it’s louder, it’s simpler and so much easier to understand.

[That’s a challenge. But it’s also an opportunity. Because if we scientists can be trained to communicate our complex science using clear language and connect with communities, we can help people understand that science is a dynamic, self‑correcting journey that empowers decisions and impacts lives.] Sadly, this is the section [in brackets above] I forget while I was delivering the talk on-stage :(

Act 9. The Impact of Having Kids

So, you might be wondering what inspired me to start training myself how to simplify and explain my science precisely 21 yrs ago? I had kids. I wanted to share my science with the little people I loved. I kept thinking to myself, “How am I going to communicate with my kids about immunology - my first true love - without the jargon?” I needed to start training myself to talk to my kids about the immune system without the technical language and jargon.From that moment on, I took on creating simplified explanations for everything related to science in general - and immunology in particular - with renewed determination.

My daughter drew this for me when she was about 10 years old and it represents to me how much she actually learned about the immune system from my simplified explanations. As you can see, she drew little green bacteria at the bottom that she named Bill. She drew B cells throwing antibody arrows at “Bill,” she drew T cells poking holes in “Bill,” and she drew a macrophage (which means big eater), the one with the very long tongue, eating “Bill.” This is exactly the way an immune response works! It’s a heated battle between the pathogen and immune system. This drawing is proof that complicated science can be broken down and explained to anyone!

Act 10. Science Communication at the Start of the Journey

My science communication journey began in earnest when I had kids, but imagine what we could do if scientists learned to communicate clearly from the start and were trained in science communication skills at the same time they were being trained in the lab to become scientists?

And that brings me to a big question that I’ve spent years thinking about: How do we turn that vision into reality? What would it take to break down the barriers and build science communication training into our system?

Let me share my vision with you…

We need to think outside the walls of academia and paywalls of science journals to create and embrace outreach opportunities. We need to add science communication skills into graduate programs - scientists in training need to learn how to develop clear and concise explanations of their science using relatable examples, analogies and storytelling to engage with the public.

I envision a world where scientists communicate their work the way a great cooking show does - think Great British Baking Show - they start by telling us what they’re making, they walk us through the ingredients, they show us all the steps and the surprises along the way. At the end they reveal the final dish and how amazing it is.

Science could do the same thing! Scientists should be encouraged to talk about their findings and how it impacts the world throughout the journey: from the very first question through every exciting twist and turn, the ups and downs, the failures and successes in the lab. Not just at the end when the science experiments are done and ready for publication but throughout the entire journey.

Why? Because science belongs to everyone.

Final Act. Closing Scene - Relabel as Science ‘Communication’ Jar

So, let’s open our science swear jars to invest in curiosity and connection within our communities. We scientists need to start using our voices to share our science with the world around us.

On the contrary to the way most academic institutions operate, communication isn’t a soft skill - it’s the strongest tool we have to turn knowledge into impact. It’s time to add science communication into science training.

Thank you!

Please watch (and share) the TEDx YouTube video to spread this message far and wide!

In my recent TEDx talk, “Confessions of a Scientist: Science Education Needs Communication Training,” I unpack the uncomfortable truth that most scientists, myself included, are never formally taught how to communicate our work to anyone outside our field.

That gap has real consequences and matters now more than ever. From classroom experiences to real-world consequences, my talk explores how better communication isn’t just a ‘soft’ skill that should be acquired on the side. Science communication skills and training are essential for fostering public trust, bridging the gap between experts and communities, and ensuring that scientific discoveries don’t just stay behind the walls of academia and paywalls of journals. Our science should be communicated in plain language to inform decisions, shape policy, and translate scientific knowledge into real-world impact that benefits society.

This talk is both a personal reckoning and a call to rethink how we train scientists and medical professionals for the world we actually live in.

YouTube: Confessions of a Scientist: Science education needs communication training

If you are so inclined, please watch, hit the ‘like’ button on YouTube, and share it far and wide with friends, family, neighbors, colleagues, your crazy uncle, people you like and maybe even people you don’t like (hee hee) – this message needs to shared far and wide and heard by everyone both on the inside and outside of science.

Later this week, I’ll break down key moments and ideas from the talk in more detail. For now, I’d love for you to watch and reflect alongside me. Let’s band together to fight for science communication skills and training to be added to graduate and medical education.

THANK YOU for being here :)

ps - the TEDx video editor chose an ‘interesting’ cover shot for the video ;)

Not sure if I was closing my eyes in deep thought or from the blinding stage lights?!

Part of the story I shared on the TEDxCU stage started 11 years ago when my daughter (at the age of 10) created a ‘science swear jar’ for me. The rule was simple: every time I started talking about science when no one asked, I had to put money in the jar - it filled up quickly! The joke, of course, is that scientists want to talk about science and often won’t stop talking about our science. Most of us are curious, passionate, and driven to share what we learn.

My ‘science swear jar’ also revealed something more serious: wanting to communicate doesn’t mean we know how to do it well.

As an immunologist and educator, I’ve spent years immersed in training programs that taught me how to think like a scientist - how to analyze data, write papers, and speak fluently in the technical language of immunology. What I didn’t learn through my 16 years of training was how to explain my work clearly to people outside my field. In fact, we’re inadvertently trained not to. The technical language or jargon becomes a badge of belonging, a signal of expertise, accuracy, and concise conversations. Over time we become very good at communicating only with one another in jargon that only we (in our specialized fields) understand.

That’s a big problem! Accuracy without clarity doesn’t build understanding or trust. Saying that vaccines “prime the adaptive immune system with an antigenic stimulus” is absolutely accurate but that means nothing to most people. On the other hand, explaining that vaccines safely train your immune system with a harmless version or piece of a pathogen (like the flu virus) so it’s ready and trained to fight the real infection is also accurate but easier to understand and connects science to lived experience.

The difference isn’t about oversimplifying - it’s about translating knowledge into meaning.

The consequences of failing to communicate with the public became painfully obvious during COVID. As evidence evolved and recommendations changed, the public questioned science more than ever. For the first time we - all os us - were living through the scientific process together. Unfortunately, no one in the scientific community explained that science is a process and that when recommendations change, it’s not because the process is broken, but because it was working exactly as intended.

During my TEDx talk, in an attempt to add clarity to the how the scientific process works through responding and updating to new evidence, I used a common item as an analogy - your GPS. Whenever our GPS reroutes us to the best possible route based on new traffic data, we all accept the update and are thankful for the new route. Science works the same way. Adaptability is a feature, now a flaw.

What the public should have heard from the scientific community was that revising conclusions in response to new data is one of science’s greatest strengths and that the process is working. Unfortunately, this message was not communicated in a way that landed with the public and without clear explanations for why the science was changing, misinformation (so much!) and confusion rushed in and eroded trust in science to an all-time low.

I’m so incredibly grateful to have had the opportunity to share my message on the TEDx stage. Science belongs to everyone, and communication is how knowledge becomes impact. If we trained scientists and physicians to communicate with the same intention that we train them to become scientists, we would change public understanding and build public trust.

I’m thankful, energized, and hopeful that this conversation continues.

photo credit to Dom Fou unsplash.com

Science communication has exploded since the COVID-19 pandemic. While Carl Sagan, PhD, MS, was the first household name in science communication, it took a long time for the field to gain traction. But with the advent of social media came a whole new platform for people to discuss their jobs, projects, and passions. It was a brand new way of exchanging information.

So when the COVID-19 pandemic hit in 2020, it was a prime opportunity for those who worked in infectious diseases, public health, and medicine to step forward. It seemed the entire world was listening, and it demonstrated both the thirst and the need for people who could effectively communicate the science. Unfortunately, the natural experiment we all lived through during the pandemic revealed just how profoundly things can unravel when science communication breaks down.

Until recently, science communication had only been given lip service in academic circles. Most universities, while nodding at the idea that researchers should be working within communities to disseminate research findings, have never explicitly encouraged or supported the practice; it’s not a skillset that is sought when hiring faculty and is not acknowledged in promotion. That has been to our detriment.

Essential Components for Science Communication Training

Scientific literacy and public trust hinge on the ability of clinicians and researchers to communicate clearly, compassionately, and credibly. Yet, medical training continues to treat science communication as a skill learned informally rather than one that is deliberately developed. Foundational abilities such as storytelling, audience analysis, and visual communication are essential for translating complex biomedical concepts into accessible, actionable information. Identifying audience needs and crafting conversations around these needs are indispensable for effectively engaging patients and non-experts alike. Science communication is not a “soft” skill, but rather how the public comes to understand, trust, and act on scientific and medical knowledge.

If we want trainees to build and use science communication skills in practice, institutions must make space for formal training in the curriculum. Further, institutions must provide support and recognize science communication work within promotion criteria. When full commitment is missing, science communication ends up scattered and inconsistent, treated as an optional extra instead of an essential part of being a well-rounded medical professional.

Communication Skills are Critical for Physicians in Training

The stakes for embedding science communication into medical education are at an all-time high. In 2025, Health and Human Services Secretary Robert F. Kennedy Jr. said, “We need to stop trusting the experts.“ To add fuel to this fire, a study from Pew Research Center indicates that trust in expertise has not rebounded to pre-pandemic levels. The media ecosystem has become incredibly noisy and as such, it’s difficult to know whom to trust and where to turn for good information. However, “A choice is not a choice when swamped with disinformation.“

The glimmer of hope is that physicians remain in a place of cultural esteem: Trust in personal physicians remains high. So it is arguably more important now than ever before to be training our physicians in science communication. Preparing future health professionals to communicate effectively with broad audiences is a public health necessity.

There is a need to revise the traditional method of training -- or lack thereof -- in science communication. Clinicians and scientists need to be formally trained to navigate uncertainty and communicate with empathy, skills that are essential for countering misinformation and rebuilding public trust in today’s fractured media landscape.

Paths to Science Communication Training

Now is the time for universities and academia at large to make science communication a part of graduate and professional training. While science communication is constantly changing with the media landscape, there are some basic pathways to start with.

Seminars/Science Communication Courses in Medical School

More institutions are beginning to offer seminars and courses in science communication, such as Vanderbilt, Johns Hopkins, and the State University of New York–Stony Brook. Requiring at least one such course in medical school would be a good way to introduce future physicians to the responsibility of communicating effectively with their patients.

Public Offerings

University-wide and even public offerings around science communication and effective ways to engage the public are a good way to connect with the broader university community. Universities sponsoring public events, even virtually, can help increase transparency and enhance trust.

Graduate Medical Education

Within graduate medical education there are various training requirements. Science communication could be one of those training areas with a certain number of hours dedicated to learning and thinking about science communication with patients throughout residency. Didactics, grand rounds, rotations, and adding science communication to scholarly activity requirements are specific areas to consider.

Creating an Experimental Space

Similar to trivia nights at local pubs and restaurants, having a monthly or bi-monthly evening where people gather to hear quick presentations in a public venue is another way to engage with the community. What might this look like in practice? When medical students, residents, fellows, and other trainees complete a research project, they then attend a “Pub Night” to discuss what they did and why it’s important to a room full of local pub-goers. Questions and feedback can be provided while workshopping ideas and presentations. It’s a unique approach to make the process of science and science communication more visible in the communities where we live and work.

Effective science communication requires training and practice. It also requires building trust, often through humanizing the people behind the science. Physicians continue to remain islands of trust in an ocean of confusion and conflicting information. Science communication is a part of their daily job. We need to start treating it accordingly.

Katie Suleta, DHSc, MPH, MS, is a public health expert and science writer specializing in epidemiology and informatics, with a focus on infectious diseases, graduate medical education, and Medicaid data.

Aimee Pugh Bernard, PhD, is an associate professor in the Department of Immunology & Microbiology at the University of Colorado (CU) Anschutz School of Medicine, assistant director of the Human Immunology & Immunotherapy Initiative, and co-director of the Colorado Clinical and Translational Sciences Institute (CCTSI) ‘Communicating Your Science to the Public’ workshop program.

Your immune system is one of the most impressive security systems on the planet. It works 24/7, never clocks out, and protects you from an invisible world of bacteria, viruses, fungi, and parasites that would love to use your body as a VRBO with their friends.

The problem? The immune system is incredibly complex, and that complexity makes it easy for misinformation and marketing scams to thrive. “Boost your immunity!” sounds great but what does that even mean?

To understand what helps your body fight disease, you need to understand the basics. And the easiest way to do that is to picture your immune system as having two main weapons:

A “shield” a.k.a. the innate immune system

A “sword” a.k.a. the adaptive immune system

Each plays a different role, and together they keep you alive.

The Shield: Your Innate Immune System

The innate immune system is your body’s first line of defense. It’s fast, automatic, and always on duty. Think of it like a shield that immediately goes up the moment danger appears.

This system doesn’t stop to ask questions. It doesn’t try to identify the intruder. It simply recognizes:

“You don’t belong here.”

Your innate immune system includes:

· Your skin, which acts like a physical wall

· Mucus in your nose and lungs that traps invaders

· Stomach acid that destroys many pathogens before they can do harm

· Immune cells like macrophages and neutrophils that patrol your body and attack (and eat) anything suspicious (kind of like Pacman)

These defenses are non-specific, meaning they respond the same way whether the invader is a cold virus, a flu virus, or a bacterium you picked up on a doorknob.

Why the ‘Shield’ Causes Symptoms

Ever wonder why you feel feverish, achy, tired, congested, or inflamed when you’re sick?

That’s not the pathogen winning. That’s your shield being raised to protect you. Fever helps slow down pathogens. Inflammation increases blood flow to the battlefield. Mucus traps invaders. Fatigue forces you to rest so your body can focus on defense. In other words, many symptoms of illness are signs that your innate immune system is doing exactly what it’s supposed to do.

When the Shield Isn’t Enough

Some pathogens are clever. They slip past the shield. They hide inside your cells. They replicate quietly before your body fully realizes what’s happening. That’s when your immune system reaches for something more precise.

That’s when the sword comes out.

The Sword: Your Adaptive Immune System

The adaptive immune system is slower to activate, but it’s incredibly smart and highly targeted. This is your body’s special forces unit.

Unlike the shield, the sword doesn’t just attack. It learns or adapts.

Once triggered, the adaptive immune system:

· Identifies the specific pathogen

· Produces antibodies that bind to it

· Flags infected cells for destruction

· Remembers the invader for the future

This system involves B cells (which make antibodies) and T cells (which help coordinate the attack and kill infected cells).

Antibodies: Tagging and Disabling the Enemy

Antibodies are like precision weapons.

They don’t usually “kill” pathogens outright. Instead, they:

· Block viruses from entering your cells

· Mark invaders so other immune cells can destroy them

Once antibodies latch on, the pathogen is effectively disarmed.

Even better? Some of those immune cells become memory cells, meaning your body remembers that pathogen. If it ever shows up again, the special forces of your immune system can respond faster and stronger.

That’s immunity.

Why Understanding Immunity Matters

Here’s where understanding the shield and sword really pays off.

You cannot “boost” your immune system like turning up the volume on a speaker. An immune system that’s too active can cause allergies, autoimmune diseases, and chronic inflammation.

What you can do is support it:

· Sleep helps immune cells communicate

· Eating a well-balanced diet including fruits and veggies

· Getting vaccines to safely train the adaptive immune system

· Staying active and getting outside

Many products promise instant immune miracles because they rely on confusion. Your immune system isn’t magic, it’s biology. And biology follows rules.

The Takeaway: Know Your Shield, Respect Your Sword

Your immune system doesn’t need hype. It needs understanding.
When you understand how these systems work together, it becomes much easier to tell the difference between real science and good marketing. If you have any concerns about your health always consult a doctor or professional.

Understanding is always the first step toward making better health decisions.

Next time you get sick, don’t panic, just think like a scientist.

For many of us in science (me included) communication about our science wasn’t something we were taught. It was something we pieced together in the cracks of our schedules, learned through trial and error, motivated by a sense of responsibility to the public and a genuine love for sharing the wonder of scientific discovery. For the past 20 years, I’ve written blogs, op-eds and guest commentaries in between experiments, answered community questions after hours and on weekends, practiced explaining my research (and everything related to vaccines) to friends and family, and hoped I was doing more good than harm.

Over time, communicating science has become embedded into my way of being as a scientist, and this commitment has naturally evolved into me being seen as the go-to person for training in science communication. As public trust in science continues to decline, the demand for clear, accessible, evidence-based communication has surged. In response, I am frequently invited to give seminars, workshops, grand rounds, and keynote speeches - far more invitations and opportunities than I have the capacity to accept. This growing need underscores both the urgency of effective science communication training and the value of cultivating scientists who can engage diverse audiences with clarity, empathy, and credibility.

From my vantage point, working at the intersection of science and public engagement, it is evident that the world has changed, and our scientific training must change with it.

Today’s scientists are expected not just to generate knowledge, but to communicate it clearly and compellingly to a wide range of audiences, including policymakers, journalists, interdisciplinary colleagues, and the public.

The stakes are high. Public health, climate change, scientific funding, biomedical innovation, and public trust in science all rely on communication that is accurate, accessible, and empathetic. Yet most emerging scientists still receive no formal preparation in these skills.

My course aims to change that.

What the Course Offers

Introduction to Science Communication provides students with the foundational skills to communicate complex ideas to diverse audiences. Through short lectures, hands‑on activities, and practical assignments, students will learn:

• The core principles of clear, accurate science communication

• How to adapt messages to different audiences

• How to build compelling narratives around scientific ideas

• The ethics of public engagement and responsible discourse

• Strategies for writing, media interviews, digital communication, and visual storytelling

By the end of the semester, students won’t just understand how to communicate, they’ll have experience doing it, tailored to diverse audiences across a variety of formats.

Why This Is a Turning Point

To me, the most significant part isn’t the course content (though I’m proud of it). It’s what this course signals: a shift toward recognizing communication as an essential scientific skill, not an optional extracurricular hobby. A shift toward valuing the time and effort scientists spend engaging with communities. A shift toward preparing trainees not only to succeed in academia, but to share the impact of their work with society.

My hope is that this course becomes the first of many and that it helps normalize the idea that scientific training includes learning to communicate with clarity and confidence to the general public. That students (and academic institutions across the globe) see science communication not as an add‑on, but as an integral part of becoming - and being - a scientist.

For immune health, some influencers seem to think the Goldilocks philosophy of “just right” is overrated. Why settle for less immunity when you can have more? Many social media posts push supplements and other life hacks that “boost your immune system” to keep you healthy and fend off illness.

However, these claims are not based on science and what is known about immune function. Healthy immune systems don’t need to be boosted or hacked. Instead, the immune system works best when it is perfectly balanced. Scientific experts on the immune system – immunologists – know that too much of an immune reaction could result in allergies, autoimmune disorders or chronic inflammation. On the flip side, too little of an immune reaction could result in illness or infection.

Your immune system requires a delicate balance to operate properly. When it’s out of balance, your immune system itself can cause disease.

Image created by copilot AI following the prompt of “create a simple image to communicate that immune health is all about balance”

Cellular balance

The immune system is the mobile defense system of your body. It is a complex network of cells and organs that work together to protect your body from infection and disease. Your immune cells are continually on patrol, traveling throughout your body looking for infectious invaders and damage.

New immune cells are created in your bone marrow. Certain immune cells – called B and T cells – are the special forces of the immune system, playing an important role in the elimination of infectious invaders. Because of this role, these cells undergo a rigorous boot camp during their development to ensure they will not discharge friendly fire on healthy cells in the body.

Any B cell or T cell exhibiting activity against the self – or autoreactivity – is killed during training. Millions of newly created B and T cells are killed every day because they fail this training process. If these self-reactive cells escape destruction, they could turn against the body and carry out an inappropriate autoimmune attack.

My research investigates how B cells are able to slip past the checkpoints the immune system has in place to guard against autoreactivity. These tolerance checkpoints ensure that autoreactive immune cells are either purged from the body or held in permanent lockdown and unable to engage in inappropriate responses that would target healthy tissue.

More isn’t necessarily better

You’ve likely seen advertisements for dietary supplements that promise to “boost immune function.” While this may sound appealing, it is important to keep in mind that the immune system functions best when perfectly balanced.

If the immune system is like a thermostat, turning it up too high results in overactivation and uncontrolled inflammation, while turning it down too low results in a failure to respond to infection and disease.

Because sustaining immune balance is critical, tinkering with the immune system through the use of supplements is not a good idea unless you have a clinical deficiency in certain vital nutrients. For people with healthy levels of nutrients, taking supplements could lead to a false sense of security, particularly since the fine print on the back of supplements usually has this disclaimer about their listed benefits: “This statement has not been evaluated by the FDA. Not intended to diagnose, treat, cure, or prevent any disease.”

Eating a well-balanced diet, exercising regularly, reducing stress and getting decent sleep, on the other hand, can help your body maintain a functioning and healthy immune system. Although these lifestyle behaviors are not foolproof, they contribute to overall good health and ultimately to a more healthy immune system.

In reality, vaccines are the only safe and effective tool beyond healthy lifestyle behaviors to support your immune system. Vaccines contain harmless forms of pathogens that help to train your immune cells to recognize and fight them. When you come into contact with the real and harmful version of the pathogen out in the wild – whether it’s at a grocery store, social event or school – at a later date, these fully trained immune memory cells will immediately begin to fight and destroy the pathogen, sometimes so quickly that you don’t even realize you’ve been infected.

In a world where people are continually bombarded by the marketing mantra that more is better, rest assured that when it comes to the immune system, maintaining perfect balance is just right.

The very beginning of my career in science is no different than my entire journey - it’s unusual. My research focused entirely on humans, not mice. This is ‘weird’ for an immunologist. Most immunologists use the traditional model system - the mouse - for most, if not all, of their experiments. I decided early on that I wanted to study the most important model system of all - the immune system within the human body. My thesis proposed that VH4.34-expressing B cells could serve as a model system for understanding B-cell tolerance in humans.

For 4.5 years, I worked seven days a week to unlock the story of VH3.34-expressing B cells. Most days I would start early in the morning (at lab by 7am) and most days I would work late into the night. I was driven by the timing of receiving human samples. If a precious human sample arrived at 2:00pm, that would be the starting point of my 12-hour protocol. It wasn’t unusual for me to eat breakfast, lunch and dinner at the lab. When I wasn’t isolating B cells from human tonsil tissue, blood, bone marrow, or spleen, I was writing up results or reading the literature to strategize my next steps. Most mornings I would wake remembering dreams where I had plotted my next set of experiments. Needless to say, I was obsessed with this project.

December 14, 2001, marked the culmination of my relentless curiosity, countless late nights in the lab, and endless experiments driven by one big question: How do human B cells learn tolerance? How do they learn to not react to the cells in our own body? Basically, how is autoimmunity - an immune response to our own tissues - averted?

visual created by copilot with the prompt, “create a visual for an instagram post to celebrate the anniversary of my PhD defense. Make a dark blue book in the center of image surrounded by festive designs to convey a celebration.”

Yes, years of immunology research has allowed us to understand there is central tolerance in the primary lymphoid organs (e.g. bone marrow and thymus) where self-reactive B cells and T cells undergo negative selection (elimination by programmed cell death) if they react to bits of self-antigen being ‘shown’ to them as a test. We also know that there are layers of tolerance in the periphery, within areas called the peripheral lymphoid organs that include the blood, lymph nodes and spleen. Yes, we know all of this at a generic level but we (immunologists) never followed a specific cell through the human body to track what happens. That’s where my model system stepped in…

My work demonstrated that VH4.34-expressing B cells are a true model of human B-cell tolerance. In healthy individuals, they tend to be suppressed or kept out of the circulating B-cell repertoire and in most cases are not allowed to progress into or beyond the germinal center. These cells only seem to escape control in individuals prone to autoimmune disease, particularly those with Systemic Lupus Erythematosus (SLE). Evidence of this comes from analyzing autoantibodies from patients with lupus. The terminal or final phase of a B cells life is to become a plasma cell, which is basically an antibody factory. You can find VH4.34-encoded autoantibodies in roughly half of lupus patients. This suggest that VH4.34-expressing B cells are allowed to progress through development in individuals with lupus. This is not true for healthy individuals. VH4.34-expressing B cells seem to be kept in check and not allowed to progress to plasma cells in healthy individuals. There is clearly some layer of tolerance – something keeping these cells from progressing – in healthy individuals that is ‘broken’ in the immune system of individuals with the autoimmune disease lupus.

If you’re curious, you can read the full story here: https://pubmed.ncbi.nlm.nih.gov/11581307/

You can also read an extension of my work here: https://pubmed.ncbi.nlm.nih.gov/15034044/

Fast forward 24 years, and I’m still passionate about science and education but my pipettes and petri dishes have been replaced with lectures that inspire the next generation of scientists and healthcare professionals. Teaching future physicians, researchers, and educators is one of the most rewarding parts of my career. I strive to help them not only understand the complexities of immunology but also appreciate the curiosity and resilience that science demands.

Beyond the classroom, I’ve embraced science communication to share the impact of science with the broader public. Science doesn’t live in isolation. Science shapes our health, our policies, and our daily lives. Through community-based conversations, public talks, and digital platforms, I strive to make science accessible, engaging, and relevant. My goal as a science communicator is to bridge the gap between scientists and society, empowering people to make informed decisions and appreciate the impact of science to improve lives and the world around us.

Cheers to the journey, the relentless curiosity that gets us out of bed every day, and the resilience that science teaches us.

photo credit to Chris Gresham-Britt at unsplash.com

At the end of The Grinch Who Stole Christmas, there’s a moment that always resonates deeply. The Grinch, having stolen every gift, ornament, and crumb of food from Whoville, waits eagerly to hear the sound of despair. Instead, he hears singing. The Whos gather in the town square, hand in hand, joyful and united. Their celebration was never about the presents; it was about something far greater: connection, meaning, and community.

Today, many of us in public health, science, and healthcare feel like the Whos. In 2025, policies have stripped away critical funding for research, decimated infrastructure for clinical trials, and slowed the development of innovative therapeutics. These losses are real and painful. They impact lives, delay progress, and threaten the future of medical discovery and the health and lives of those who are sick and in need.

But you know what cannot be stolen? Our purpose.

Science is not defined by budgets alone. It is driven by curiosity, collaboration, and an unwavering commitment to improving lives. Public health is not a line item—it is a calling. Even in the face of adversity, we remain steadfast because our work is rooted in something bigger than politics or profit. It is rooted in care.

Like the Whos, we will keep singing. We will keep teaching, researching, and advocating. We will find creative ways to collaborate across institutions, disciplines, and borders. We will mentor the next generation of scientists and clinicians, ensuring that the flame of discovery never goes out. We will continue to fight for evidence-based policies and equitable access to care, because these values are the heart of our mission.

The Grinch learned that Christmas “doesn’t come from a store.” Likewise, progress in health and science doesn’t come solely from funding (although essential) - it comes from the people. People who believe in the power of knowledge to heal, who refuse to let setbacks define the future, and who understand that the strength of our community lies in our shared commitment to humanity.

So, yes, the road ahead may be harder. But we are not broken. We are connected by our love of caring for others, by our drive to discover, and by the collaborations that make innovation possible. No administration can steal that. No policy can erase that.

Let’s keep singing together.

photo credit to Tim Marshall at unsplash.com

Every day, your immune system performs a delicate balancing act, defending you from thousands of pathogens that cause disease while sparing your body’s own healthy cells. This careful equilibrium is so seamless that most people don’t think about it until something goes wrong.

Autoimmune diseases such as Type 1 diabetes, lupus and rheumatoid arthritis are stark reminders of what happens when the immune system mistakes your own cells as threats it needs to attack. But how does your immune system distinguish between “self” and “nonself”?

The 2025 Nobel Prize in physiology or medicine honors three scientists – Shimon Sakaguchi, Mary Brunkow and Fred Ramsdell – whose groundbreaking discoveries revealed how your immune system maintains this delicate balance. Their work on two key components of immune tolerance – regulatory T cells and the FOXP3 gene – transformed how researchers like me understand the immune system, opening new doors for treating autoimmune diseases and cancer.

How immune tolerance works

While the immune system is designed to recognize and eliminate foreign invaders such as viruses and bacteria, it must also avoid attacking the body’s own tissues. This concept is called self-tolerance.

For decades, scientists thought self-tolerance was primarily established in the parts of the body that make immune cells, such as the thymus for T cells and the bone marrow for B cells. There, newly created immune cells that attack “self” are eliminated during development through a process called central tolerance.

However, some of these self-reactive immune cells escape this process of elimination and are released into the rest of the body. Sakaguchi’s 1995 discovery of a new class of immune cells, called regulatory T cells, or Tregs, revealed another layer of protection: peripheral tolerance. These cells act as security guards of the immune system, patrolling the body and suppressing rogue immune responses that could lead to autoimmunity.

Image from © The Nobel Committee for Physiology or Medicine. Ill. Mattias Karlén

While Sakaguchi identified the cells, Brunkow and Ramsdell in 2001 uncovered the molecular key that controls them. They found that mutations in a gene called FOXP3 caused a fatal autoimmune disorder in mice. They later showed that similar mutations in humans lead to immune dysregulation and a rare and severe autoimmune disease called IPEX syndrome, short for immunodysregulation polyendocrinopathy enteropathy X-linked syndrome. This disease results from missing or malfunctioning regulatory T cells.

In 2003, Sakaguchi confirmed that FOXP3 is essential for the development of regulatory T cells. FOXP3 codes for a type of protein called a transcription factor, meaning it helps turn on the genes necessary for regulatory T cells to develop and function. Without this protein, these cells either don’t form or fail to suppress harmful immune responses.

Harnessing the immune system for medicine

Regulatory T cells can be heroes or villains, depending on the context. When regulatory T cells don’t work, it can lead to disease. A breakdown in immune tolerance can result in autoimmune diseases, where the immune system attacks healthy tissues. Conversely, in cancer, regulatory T cells can be too effective in suppressing immune responses that might otherwise destroy tumors.

Understanding how FOXP3 and regulatory T cells work launched a new era in immunotherapies that harness the immune system to treat autoimmune diseases and cancer. For autoimmune diseases such as rheumatoid arthritis and Type 1 diabetes, researchers are exploring ways to boost the function of Tregs. For cancer, the goal is to inhibit Tregs, allowing the immune system to target tumors more aggressively.

Beyond disease treatment, this research may also improve organ transplantation, where immune tolerance is crucial to prevent rejection. Scientists are exploring how to engineer or expand Tregs to help the body accept transplanted tissues over the long term.

Continuing to unlock the secrets of immune regulation can help lead to a future where the immune system can be precisely tuned like a thermostat – whether to turn it down in autoimmunity or rev it up against cancer.

The 2025 Nobel Prize reminds us that science, at its best, doesn’t just explain the world – it changes lives.

This article is republished from The Conversation under a Creative Commons license.

Titled “From Data to Dialogue: Science Communication for the Real World,” the retreat offered PhD candidates and postdoctoral scholars the opportunity to explore how to make their science more accessible, engaging, and impactful. By emphasizing the importance of building authentic connections with the community, participants learned how to communicate their research in ways that resonate with diverse audiences and contribute meaningfully to public understanding and trust in science.

The day was structured around several interactive sessions, each designed to equip participants with practical tools and strategies to elevate their communication skills:

The Art of Making Science Interesting and Relatable to the General Public
I started the retreat by sharing my top 10 tips for how to make complex science relatable and compelling. From knowing your audience to removing jargon to using analogies, we discussed ways to distill dense data and complex science into digestible narratives. Participants were also given the opportunity to craft and share their own elevator pitches—concise, engaging summaries of their research designed for non-expert audiences.

From Conflict to Connection: Navigating Mis- and Disinformation with Clarity and Compassion
The ability to address misinformation and disinformation has become increasingly important as the digital landscape is changing how everyone accesses and receives information. In today’s new world, scientists are increasingly called upon to address mis- and disinformation, whether or not they are willing and prepared to do so. Throughout this session we explored how to engage in respectful, empathetic conversations that prioritize connection over correction. I aimed to empower the next generation of scientists to become trusted voices in their communities capable of fostering understanding, dispelling myths, and building bridges between science and society through clarity and connection.

The Power of Storytelling and Crafting a Compelling Research Narrative
Every research project has a story that is capable – if thoughtfully crafted - to captivate, educate, and inspire its audience. During this session, we worked on identifying the “why” behind each participant’s work and practiced weaving it into narratives that resonate with broader audiences. By framing their research through the lens of the hero’s journey—complete with challenges, discoveries, and transformation—participants learned how to craft compelling stories that not only inform but inspire.

Expanding Your Reach Beyond the Walls of Academia and Paywalls of Journals
Finally, we discussed how to share science beyond the confines of academic journals and conferences. From podcasts and in-person public talks to platforms like Substack and local news outlets, we explored the many avenues available for scientists to amplify their voices and connect with diverse communities. Additionally, I emphasized the importance of leveraging social media platforms to significantly expand our reach. It is up to the next generation of scientists to meet the public where they are to communicate science. At this moment in time most people 30 and under get their “news” from social media. To reach and connect with the general public, scientists must embrace social media to foster dialogue and build communities around science.

Throughout the day, I was struck by the thoughtful questions and genuine desire to grow as communicators. It reminded me why I do this work and why it matters so much. It was truly inspiring to see the next generation of scientists so invested in building bridges between the lab and the public.

Returning to Rochester as a facilitator rather than a student was a full-circle moment. It was a privilege to contribute to the professional development of the next generation of scientists and to witness firsthand the momentum building around science communication in academia.

I left the retreat energized and hopeful. If these trainees are any indication, the future of science and science communication is in excellent hands.

In a time when health information is abundant yet often conflicting, and medical decisions feel increasingly complex, the Denver Museum of Nature and Science invited community members to join together for an evening focused on inspiration, curiosity, and open dialogue. Hosted by the Institute for Science and Policy, the event centered around the premiere of The Plea, a new short documentary by filmmaker Neil Halloran. The film chronicles one of humanity’s greatest public health triumphs: the eradication of smallpox—the only human disease ever eliminated through science and global cooperation.

Following the screening, I had the honor of joining a town-hall style panel discussion alongside Neil Halloran, the documentary film maker, Dr. David Higgins, a pediatrician, and Dr. Cynthia Hazel, a public health expert. Together, we explored the themes of trust in science, the power of storytelling in science, the controversy surrounding vaccines, and the role of public health in shaping our collective future.

A Triumph of Science and Solidarity

As an immunologist, mother of two, and educator, I was deeply moved by The Plea. The story of smallpox eradication is not just a scientific milestone—it’s a testament to what humanity can achieve when we trust science and work together across borders, cultures, and ideologies. It’s easy to forget that just a few generations ago, smallpox claimed millions of lives. Today, thanks to rigorous research, coordinated global efforts, and widespread vaccination, it exists only in history books.

Moments like these remind us of the incredible power of science—not just to understand the world, but to change it for the better.

The Panel: Navigating Trust and Complexity in Modern Public Health

Our panel discussion touched on many pressing issues, including the erosion of public trust in science and expertise. The COVID-19 pandemic laid bare the challenges of communicating complex scientific information in a rapidly evolving landscape. Misinformation spread faster than viruses, and many communities were left feeling confused, skeptical, or even betrayed.

I shared my perspective on how far we’ve come in terms of medical progress—from the development of mRNA vaccines to the near-elimination of diseases like polio—and how far we’ve fallen in terms of public trust. As an educator and science communicator, I see firsthand how critical it is to listen to and engage with the public, answer questions honestly and with empathy, and foster curiosity rather than fear.

Science is not static. It evolves. And that evolution requires humility, transparency, and dialogue.

Rebuilding Trust Through Engagement and Education

One of the most powerful aspects of the event was its format: a town-hall style conversation that invited audience members to ask questions, share concerns, and engage directly with experts. This kind of open, respectful dialogue is exactly what we need to rebuild trust in science.

I emphasized the importance of science communication—not just in classrooms and journals, but out in the community in museums and libraries as well as online spaces like social media and websites. When we make science accessible and human, we empower people to make informed decisions and become active participants in their own health and well-being.

To further this mission, I’m proposing to launch a dedicated science communication program at the medical campus where I teach. This initiative—if given the green light—will provide formal training to both emerging scientists and healthcare providers, as well as those already established in their careers. Despite its critical role in public engagement and trust-building, science communication remains an underdeveloped skill in many academic and professional settings.

I firmly believe that effective science communication is no longer optional—it is a responsibility we must embrace. Scientists need to get out in the community… move our science beyond the walls of academia and the paywalls of journals, and publish our research in plain language, jargon-free summaries on open access websites where people can interact and ask questions. As scientists and healthcare professionals, I believe we have a responsibility to communicate science with clarity, compassion, and confidence—especially when our communities need answers most.

Looking Ahead: Collaboration Is Key

The eradication of smallpox was not just a medical achievement—it was a global collaboration. And if we hope to tackle future challenges—from emerging diseases to food safety to climate-related health threats—we must embrace that same spirit of cooperation.

Trust in science doesn’t happen overnight. It’s built through relationships, transparency, and shared goals. Events like this are a step in the right direction.

Final Thoughts

I left the museum last evening feeling hopeful. Despite the challenges ahead, the passion and curiosity in the room were palpable. People want to understand. They want to engage. And they want to be part of the solution.

Science has the tools to solve our greatest problems. But it’s up to all of us—scientists, educators, filmmakers, physicians, and community members—to ensure those tools are used wisely, ethically, and inclusively.

Let’s keep the conversation going.

One final note, if you haven’t watched it already, please consider watching the powerful documentary The Plea, available on YouTube. Your perspective on the triumph of science and global collaboration will likely be expanded in ways you didn’t expect.