Immunology

Excited to share the immunology content guidelines for medical education with the members of the Immunology Teaching Interest Group (ITIG) today at the American Association of Immunologists (AAI) conference. This was a 3-year endeavor with a large task force of dedicated immunology educators that will be published in ImmunoHorizons soon. Thankful to everyone who made this work possible and the support of the AAI Education Committee.
Nicholas Pullen Vijaya Knight (Nagabhushanam) Scott Thompson Michelle Swanson-Mungerson Jennifer Grier Tim Bauler Zhao Yuan Pooja Jain The American Association of Immunologists

Recent research has demonstrated that immune system aging differs significantly between women and men. Analysis of blood samples from nearly 1,000 adults revealed that women experience more pronounced age-related changes, including increased inflammatory immune cells, which may contribute to higher rates of autoimmune diseases, particularly after menopause. In contrast, men exhibit less extensive changes but show an increase in blood cells with pre-leukemia alterations, potentially explaining higher rates of certain blood cancers. These findings highlight the importance of considering biological sex in precision medicine and developing tailored strategies for healthy aging.

Headed to AAI? Don't miss out on all the amazing EDUCATION SESSIONS!
Don't forget to add the Immunology Teaching Interest Group Session on Friday, April 17 in Room 153C from 8-10am to your schedule!
I'll be sharing the findings from the AAI Medical Immunology Task Force in my talk, 'Establishing AAI-Recommended Immunology Content Guidelines for Medical Education in the USA.'
You'll also be able to read about it in ImmunoHorizons - publication coming soon!
Nicholas Pullen

🚨 What if a single immune cell could kill, trap, signal, and even sacrifice itself—all within minutes of infection?🧬🔥
Meet neutrophils — the most abundant and arguably the most underestimated warriors of our immune system.
These cells aren’t just first responders—they are multi-functional combat units executing a coordinated defense strategy:
🔬 Phagocytosis – The Rapid Kill Mechanism
Neutrophils engulf and destroy pathogens within minutes.
📊 Studies show they can phagocytose microbes within 5–10 minutes of encountering them (Kolaczkowska & Kubes, 2013).


🕸️ NETosis – The Ultimate Trap Strategy
They release Neutrophil Extracellular Traps (NETs)—DNA webs laced with antimicrobial proteins.
📊 NETs can immobilize and kill pathogens extracellularly, reducing microbial spread by up to 90% in localized infections (Brinkmann et al., 2004).


💣 Degranulation – Chemical Warfare
Neutrophils release enzymes like elastase and myeloperoxidase.
📊 These enzymes contribute to direct microbial killing and tissue-level pathogen clearance (Borregaard, 2010).


📡 Cytokine Production – Immune System Communication Hub
They secrete cytokines and chemokines to recruit other immune cells.
📊 Neutrophils can produce over 20 different signaling molecules, shaping both innate and adaptive immunity (Tecchio et al., 2014).


⚡ Reactive Oxygen Species (ROS) – Molecular Destruction
Neutrophils generate ROS to destroy pathogens at the biochemical level.
📊 The “respiratory burst” can increase oxygen consumption by up to 10–20 fold during infection (Nathan, 2006).



📊 The Bigger Picture
• Neutrophils make up 50–70% of all circulating white blood cells (Rosales, 2018)
• The human body produces ~100 billion neutrophils daily to maintain immune readiness
• Their lifespan is short—~5–90 hours, yet their impact is immediate and powerful



⚠️ But here’s the twist…
When dysregulated, these same mechanisms contribute to:
➡️ Chronic inflammation
➡️ Autoimmune diseases
➡️ Tissue damage & cancer progression



💡 Final Insight:
Neutrophils are not just defenders—they are precision-engineered immune machines, balancing destruction and communication to protect the body in real time.

👨‍🔬 Curated by Dip Ghosh

#Immunology #Neutrophils #InnateImmunity #MedicalScience #Biotechnology #Research #Healthcare #LifeSciences #ScienceCommunication

👉If you’re enjoying the content and want to support me, consider following:
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[#PARCC Highlight]: Les cellules NK, nouvelles cibles pour protéger le cœur après un infarctus !
L'insuffisance cardiaque post-infarctus reste un défi médical de taille. L'équipe de Hafid Ait-Oufella au #PARCC vient de publier une étude majeure qui change notre regard sur les mécanismes immunitaires de la réparation cardiaque.

🔬 Qu’est-ce qui est démontré ?
Jusqu'ici, le rôle des cellules Natural Killer (NK) restait flou dans les maladies cardiaques. Cette étude démontre que :
  📍  Après un infarctus, les cellules NK sont recrutées vers le cœur (via l'axe CCR2) et libèrent du granzyme B, provoquant la mort des cardiomyocytes.
   📍 Elles stimulent la production de cellules inflammatoires myéloïdes dans la moelle osseuse (via le GM-CSF).
   📍 La déplétion de ces cellules réduit l'inflammation et améliore significativement la fonction cardiaque.

🌟 Pourquoi c’est important ?
📌 Les cellules NK deviennent une cible innovante pour de futurs traitements immunomodulateurs.
📌 L'identification d'une signature transcriptomique chez l'humain confirme le potentiel thérapeutique de cette découverte.
📌 Cette étude ouvre la voie à des stratégies d'immuno-thérapie pour limiter les séquelles et prévenir l'insuffisance cardiaque chronique.

🤝 Une synergie d'expertise au PARCC, ce travail n'aurait pu voir le jour sans une collaboration étroite entre plusieurs équipes du PARCC : les équipes de Jean-Sébastien Silvestre & Jean-Sébastien Hulot, Clément Cochain et Alexandre Loupy

👏 Félicitations à tous et également à tous les collaborateurs pour ce magnifique succès collectif ! 👏

Raphaël Cohen-Belmatoug Vincent Duval Rida Al-Rifai Icia Santos Zas Charlène Jouve Sara Thietart Théo Guyon Marie Piollet Soraya Taleb Eric Vivier Giuseppe Rizzo Olivier Hermine Sikander Hayat
Faculté de Santé - Université Paris Cité Inserm Paris / Île-de-France Tatiana Monseur Mohamed ABOU ALI POLYGON Therapeutics

🔗 Pour en savoir plus: https://lnkd.in/eqUEnvtU

#Cardiology #Research #NatureCommunications #PARCC #Inserm #UPCité #HeartFailure #Immunology #ScienceInnovation

I’ve caught cod for years.

Turns out they’ve been quietly ignoring half of immunology.

Unlike most fish species, Atlantic cod lack MHC class II and do not have classical CD4⁺ T-cell responses. That’s a big chunk of what we normally consider essential adaptive immunity.

And yet… they’re doing absolutely fine.

Instead, they’ve expanded other arms of the immune system and rewired how it works.

Maybe “essential” in immunology just means “essential in the systems we happen to study.”

https://lnkd.in/evmz8ypF

Mycobacterium tuberculosis (M.tb) is a bacterial pathogen that has evolved in humans, and its interactions with the host are complex and best studied in humans.

Myriad immune pathways are involved in infection control, granuloma formation, and progression to tuberculosis (TB) disease. Inflammatory cells, such as macrophages, neutrophils, conventional and unconventional T cells, B cells, NK cells, and innate lymphoid cells, interact via cytokines, cell-cell communication, and eicosanoid signaling to contain or eliminate infection but can alternatively mediate pathological changes required for pathogen transmission. Clinical manifestations include pulmonary and extrapulmonary TB, as well as post-TB lung disease.

Risk factors for TB progression, in turn, largely relate to immune status and, apart from traditional chemotherapy, interventions primarily target immune mechanisms, highlighting the critical role of immunopathology in TB.

Maintaining a balance between effector mechanisms to achieve protective immunity and avoid detrimental inflammation is central to the immunopathogenesis of TB. Many research gaps remain and deserve prioritization to improve our understanding of human TB immunopathogenesis.

Learn more in #ScienceImmunology on #WorldTBDay: https://scim.ag/4iME6wt

What if aging is, in part, an immune system problem?

Yesterday, I shared that the thymus - long thought to be a "forgotten organ" in adults - may actually be a critical driver of immune resilience.

Today, let’s dive into the data from our first Nature paper to see exactly how much it matters and what drives its decline.

To figure out if thymic health impacts adult longevity, we developed a deep learning system to quantify thymic functionality from routine CT scans. We analyzed over 27,000 asymptomatic adults from two prospective and independent cohorts (the National Lung Screening Trial and the Framingham Heart Study).

The results were striking. We found that the rate of thymic decay is highly individualized - and losing that thymic tissue forecasts a significantly higher risk of disease and death.

👉 Here is what the data showed for individuals with high thymic health compared to those with low thymic health:

- All-cause mortality: An approximately 50% reduction in the risk of death over a 12-year follow-up.
- Cancer: A 36% lower likelihood of developing lung cancer, and nearly a 50% lower likelihood of dying from it. We also saw lower pan-cancer mortality overall.
- Cardiovascular Disease (CVD): Massive risk reductions in CVD mortality ranging from 63% to 92% across the cohorts.
- Other diseases: Mortality from pulmonary diseases was 61% lower, and mortality from endocrine/metabolic diseases was 68% lower.

👉 But here is the also a potential actionable part: Thymic decay isn't just an unavoidable part of aging - it might be tied to how we live.

- Metabolic Health: High-density lipoprotein (HDL) showed a significant positive association with thymic health. Conversely, higher BMI, triglycerides, fasting glucose, and blood pressure were negatively associated with it.
- Lifestyle: Smoking intensity and duration had a strong negative impact on the thymus.
- Inflammation: Participants with chronic systemic inflammation (consistently high CRP levels) or elevated pro-inflammatory proteins (like IL-6 and IL-18) had substantially lower thymic health.

👉 These findings challenge the dogma that the adult thymus is just leftover fatty tissue. If this holds, it positions the thymus as a central regulator of disease susceptibility in adulthood.

Even better, it suggests that actionable lifestyle choices — like smoking reduction, weight loss, and managing inflammation — could potentially preserve or improve our thymic health.

Read the full open-access study here: https://lnkd.in/ePyWdTAM

#Immunology #Longevity #Nature #Aging

The thymus, long considered virtually inactive in adulthood—at least that’s how it was presented to me when I was a young medical student—is now confirmed to play a central role in our health and longevity

Numerous studies over the past several years have demonstrated its important role in adults, notably a study published in the NEJM in 2023 that showed the deleterious impact of thymectomy in adults (Kooshesh et al, N Engl J Med 2023 DOI: 10.1056/NEJMoa2302892)

This article published in Nature confirms the importance of the “gland of the soul” (the etymology of “thymus” in Greek) in adults. By analyzing more than 27,000 adults from large cohorts, the authors show that the functional state of the thymus—measured using an innovative artificial intelligence approach applied to CT scans—is strongly associated with the risk of mortality and major diseases.

The results are particularly striking:

Individuals with better “thymic health” have an approximately 50% lower overall risk of death, as well as a significant reduction in the risk of cancer and cardiovascular disease. These associations persist regardless of age, sex, smoking status, or comorbidities, suggesting that the thymus remains a key player in immunity well beyond childhood.

The study also highlights a close link between the thymus, chronic inflammation, and metabolism. Poor thymic health is associated with unfavorable inflammatory profiles, obesity, smoking, and a less healthy lifestyle. Conversely, certain modifiable factors such as physical activity or good metabolic balance appear to preserve its function.


This research reposition the thymus as a major regulator of immune aging. Above all, it opens up significant avenues for further research: better understanding the factors driving its decline, identifying preventive measures, and perhaps one day developing strategies for “immune rejuvenation.” It is worth noting here the likely significant role of obesity, as excess fat in the gland has particularly deleterious effects, and there are interesting studies exploring various strategies involving IL-7, growth hormone, and others.

Ultimately, this study reminds us of the importance of our immune system throughout life and also not to neglect organs considered, without good reason, to be useless. We could also cite interesting studies—even if the impact is less significant than that of the thymus—on the importance, for example, of the tonsils and adenoids or the appendix.

Magali Irla Clémence Granier Daniel Olive

#thymus #health

https://lnkd.in/eEJkY_tE

Over the last few months I had the privilege of working together with Victor Appay and Takuya Yamamoto on a review regarding the central importance of CD8⁺ T cells in controlling both acute and chronic viral infections. I am very excited to share that the review is now published in Nature Reviews Immunology.
We discuss qualitative attributes associated with CD8+ T cell efficacy and propose tailored approaches towards interventional strategies
https://lnkd.in/emEYn_Nd
Hope this is helpful both for people working on this field and new comers 😀
#CD8_T_cells_are_cool

#RHIVIERA #ERASE_HIV
Nature Portfolio Institut Pasteur ANRS Maladies infectieuses émergentes The EU2Cure Consortium

Great news: A new opportunity in immunology education in Portugal! 🎓✨
Find out more information on the Master in Integrative and Systems Immunology (MISI) here ⬇️

How is our understanding of immune memory evolving? Check out our special issue on immune memory, with a beautiful cover from Ester Marina Zárate, PhD from Shane Crotty's lab! The various components and layers of immune memory are depicted as a music emanating from an orchestra, highlighting the importance of coordination and harmonization of the many facets of immune memory—both innate and adaptive—for effective and lasting immune protection. https://lnkd.in/eKp9q3tH

Long considered a cornerstone of protective immunity, immune memory is now being redefined, extending beyond classical adaptive responses to encompass broader, long-lasting changes across the immune system.

In the new Immunity special issue, eight perspectives explore the roles of innate and adaptive memory, from T cells and antibodies to trained immunity and aging. Together, they highlight immune memory as a coordinated, dynamic system, more like an orchestra than a single pathway, shaping effective and lasting protection.

Check out the entire April issue out now, just in time for #IMMUNOLOGY2026 #AAI2026! The American Association of Immunologists

Andrew Oberst Stephen Tait Deepta Bhattacharya Stephen Jameson Sara Hamilton Laura Mackay Thomas Burn Marcus Buggert Claire Gustafson, Ph.D. Joel G. Rurik, PhD Sarah Adamo Luis Barreiro Raúl Aguirre-Gamboa

Immunity is the body's ability to recognize, neutralize, and eliminate harmful foreign substances—such as bacteria, viruses, and toxins—to protect against disease.
This complex defense system is generally categorized into two main branches: Innate and Acquired (Adaptive) immunity.
1. Innate Immunity (Non-Specific)
This is the defense system you are born with. It provides an immediate, "first-line" response to any invader, regardless of what it is.
Physical Barriers: Skin, mucous membranes, and cilia (tiny hairs in the airways).
Chemical Barriers: Stomach acid, enzymes in saliva and tears.
Cellular Defenses: White blood cells like neutrophils and macrophages that engulf and destroy pathogens.
2. Acquired Immunity (Adaptive)
This type of immunity develops throughout your life as you are exposed to diseases or receive vaccines. It is highly specific and "remembers" pathogens for future encounters.
A. Active Immunity
This occurs when your own immune system produces antibodies in response to a pathogen.
Natural Active: Developing immunity after recovering from an infection (e.g., getting chickenpox once).
Artificial Active: Developing immunity via a vaccine (e.g., a flu shot).
B. Passive Immunity
This occurs when you are given antibodies rather than producing them yourself. It provides immediate protection but is temporary.
Natural Passive: Antibodies passed from a mother to her baby through the placenta or breast milk.
Artificial Passive: Receiving an injection of antibodies (e.g., anti-venom for a snake bite or immunoglobulin therapy).
#Biotechnology #SBvvip

For years, CCR5 has been discussed mostly in silos.

HIV people know it as a co-receptor.
Oncology people see it through the tumor microenvironment.
Neurobiology is now showing it may also matter in how injured or malignant tissue stabilizes pathological signaling.

This paper argues that CCR5 is better understood not as a disease-specific target, but as a context-dependent signaling axis that helps organize cell trafficking, intercellular communication, and persistence across biological systems.

In other words:

Different diseases.
Shared signaling logic.

That shift matters, because once you stop viewing disease only through isolated components and start looking at the communication architecture underneath, new therapeutic questions open up.

I’ve posted the paper here as a PDF.
Zenodo link in the comments.

#CCR5
#SystemsBiology
#Immunology
#Oncology
#Neurobiology
#TranslationalMedicine

The OX40/OX40L Axis Promotes Th2 Activity and Impairs Regulatory T Cell Function in Atopic Dermatitis. First author: Kazuhiko Yamamura; corresponding author: Emma Guttman-Yassky


Read the article here: doi.org/10.1111/all.70252


Atopic dermatitis (AD) patients show marked OX40 upregulation in effector and regulatory CD4+ T cells. Interaction with OX40L impairs Treg suppressive function, thereby sustaining Th2 activity and promoting inflammation. Thus, the OX40/OX40L axis drives impaired immune regulation and contributes to enhanced skin inflammation in AD.

#Allergy_journal
Read more articles published in #Allergy on #atopicdermatitis here: https://lnkd.in/dvN_pd2

Vitiligo is an autoimmune disease of melanocyte destruction, which manifests as progressive, patchy loss of pigmentation in the skin. As one of most common autoimmune diseases, vitiligo inflicts a significant psychosocial burden. Research over the past two decades has revealed the underlying immune mechanisms of vitiligo, with key studies combining detailed analyses of patient tissue samples with mechanistic experiments in mouse models. Vitiligo has emerged as a prototypical CD8+ T cell-mediated autoimmune disease, with cooperation between innate immune cells, dendritic cells, T cells, keratinocytes and fibroblasts driving autoimmune pathology against the uniquely susceptible melanocyte target. The study of vitiligo has also revealed aspects of CD8+ T cell memory and resident memory against self-antigens. This work has drawn from, and contributed to, the study of melanoma immunology. Whereas drugs used for other autoimmune conditions have been largely ineffective in treating vitiligo, a growing base of knowledge recently led to the first successful FDA-approved immune-modulating drugs for vitiligo. This review focuses on the immunology of vitiligo: the mechanisms that drive melanocyte destruction, the biology of aberrant T cell responses against melanocytes and therapeutic means for counteracting this autoimmune condition. This Review from Turk and Huang discusses the immune processes involved in the development of vitiligo, an autoimmune disease in which melanocyte destruction causes loss of skin pigmentation. The authors highlight key studies from the past two decades that have shaped our understanding of vitiligo and led to newly approved immune-modulating drugs for the disease.

🛡️ IMMUNE SYSTEM – COMPLETE ANATOMY
🔹 What is Immune System?
The immune system is the body’s defense system that protects against:
Bacteria 🦠
Viruses 🧬
Fungi 🍄
Parasites 🐛
👉 It identifies “self” vs “non-self” and destroys harmful invaders.
🧠 1. MAIN COMPONENTS
🔬 A. Primary Lymphoid Organs
Where immune cells are formed & matured:
✅ Bone Marrow
Produces all blood cells
B-cells mature here
✅ Thymus
T-cells mature here
Active mainly in childhood
🧪 B. Secondary Lymphoid Organs
Where immune response happens:
Lymph nodes
Spleen
Tonsils
Peyer’s patches (intestine)
🧬 2. TYPES OF IMMUNITY
🔹 1. Innate Immunity (Natural)
Present from birth
Fast response
Examples:
Skin barrier
Stomach acid
White blood cells
🔹 2. Adaptive Immunity (Acquired)
Develops over time
Specific + memory-based
Types:
Active (infection/vaccine)
Passive (mother antibodies)
🧪 3. IMMUNE CELLS
🧫 White Blood Cells (WBCs)
🔥 Neutrophils
First responders
Kill bacteria
🧬 Lymphocytes
B-cells → produce antibodies
T-cells → kill infected cells
🧹 Macrophages
Eat pathogens (phagocytosis)
⚔️ Natural Killer (NK) Cells
Kill virus-infected cells
🧴 4. ANTIBODIES (IMMUNOGLOBULINS)
Produced by B-cells
IgG → long-term protection
IgA → mucosal surfaces
IgM → first response
IgE → allergies
IgD → B-cell function
🔥 5. IMMUNE RESPONSE (STEP-BY-STEP)
Pathogen enters body
Recognized as foreign
WBCs activated
Antibodies produced
Pathogen destroyed
Memory cells formed
👉 Next time → faster response ⚡
⚙️ 6. IMPORTANT FUNCTIONS
Protects from infections
Removes dead cells
Fights cancer cells
Creates memory for future protection
🧪 7. COMMON DISORDERS
🔴 Autoimmune Diseases
Body attacks itself
Example: Rheumatoid arthritis
🔴 Immunodeficiency
Weak immune system
Example: HIV/AIDS
🔴 Allergies
Overreaction to harmless substances
🧾 QUICK SUMMARY
FeatureImmune SystemFunctionDefenseCellsWBCsOrgansBone marrow, thymus, lymph nodesTypesInnate & Adaptive

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𝐂𝐃𝟕𝟎 𝐢𝐬 𝐞𝐯𝐞𝐫𝐲𝐰𝐡𝐞𝐫𝐞 𝐢𝐧 𝐬𝐨𝐥𝐢𝐝 𝐭𝐮𝐦𝐨𝐫𝐬. 𝐖𝐞 𝐣𝐮𝐬𝐭 𝐰𝐞𝐫𝐞𝐧'𝐭 𝐬𝐞𝐧𝐬𝐢𝐭𝐢𝐯𝐞 𝐞𝐧𝐨𝐮𝐠𝐡 𝐭𝐨 𝐬𝐞𝐞 𝐢𝐭.

In solid tumors, antigen heterogeneity remains a fundamental obstacle. When a target is expressed on only a fraction of tumor cells, CAR T cells eliminate that fraction. The rest survives, proliferates, and drives relapse.

CD70 has long been considered a promising solid tumor target: aberrantly expressed in kidney, ovarian, and pancreatic cancers, while physiologically restricted to activated immune cells. But its heterogeneous expression pattern has limited clinical responses so far.

A new study from Sophie Hanina and al. challenges the way we read that heterogeneity.

𝐓𝐡𝐞 𝐜𝐨𝐫𝐞 𝐡𝐲𝐩𝐨𝐭𝐡𝐞𝐬𝐢𝐬
What if CD70-negative tumor cells aren't truly negative but simply below the detection threshold of conventional methods and conventional CARs?

𝐖𝐡𝐚𝐭 𝐭𝐡𝐞𝐲 𝐟𝐨𝐮𝐧𝐝
🔹 Conventional CD70-CAR T cells selectively killed CD70-high cells and left CD70-low/negative cells untouched, mirroring the modest clinical response rates observed in trials.
🔹 CD70-negative tumor cells were not truly negative. EZH2-mediated H3K27me3 histone trimethylation epigenetically silenced CD70 but incompletely, allowing residual low-level expression to persist across all tumor cells.
🔹 CD70 chromatin accessibility, profiled at single-cell resolution in primary patient tumors, revealed the same epigenetic signature as in PDX models, supporting the existence of pan-cellular, low-level CD70 expression in apparent CD70-negative patient tumors.

𝐄𝐧𝐭𝐞𝐫 𝐭𝐡𝐞 𝐇𝐈𝐓 𝐫𝐞𝐜𝐞𝐩𝐭𝐨𝐫
An HLA-independent T cell (HIT) receptor signals through the CD3 complex, conferring superior sensitivity to low antigen densities.

CD70-HIT T cells, co-expressing CD80 and 4-1BBL for costimulation:
✔ Completely eradicated CD70-heterogeneous tumors across all three cancer models
✔ Showed no greater toxicity than conventional CD70-CAR or CD19-CAR T cells in cytotoxicity assays and in a humanized in vivo model
✔ Spared normal adult tissues, where CD70 chromatin accessibility was largely absent outside activated immune cells

𝐖𝐡𝐚𝐭 𝐭𝐡𝐢𝐬 𝐫𝐞𝐝𝐞𝐟𝐢𝐧𝐞𝐬
Tumor antigen heterogeneity has been framed as a binary problem: cells are either positive or negative. This study reframes it as an epigenetic spectrum and shows that the right receptor design can exploit that spectrum therapeutically.

CD70 may not be a heterogeneous target after all. It may be a pan-cellular target that requires a pan-sensitive receptor.

💬 Has the field been chasing new targets when existing ones just needed a more sensitive receptor? As receptor design becomes more sophisticated, how does this redefine what we manufacture and how we validate it?

📕 Link to the paper in the comments.

THYMIC HEALTH IS IN!

For a long time, it has been widely assumed that the thymus plays an important role in childhood, helping build the immune system, and then quietly fades into irrelevance in adulthood. That story is incomplete.

Over the past few years, my colleagues and I set out to revisit this question. The result is something I am both humbled and proud to share: two papers published in Nature, in the same issue, exploring the role of thymic health in adulthood. Beyond the academic milestone, this work represents a shift in how we understand the immune system, aging, and disease risk.
At its core, the message is simple. The thymus does not stop mattering when we grow up. In fact, it may be a key yet overlooked regulator of long-term health.

In our first study, we analyzed more than 27,000 individuals across large, prospective cohorts of generally healthy adults. We found that thymic health varies widely between people of the same age, and that this variation is strongly associated with meaningful outcomes. Individuals with higher thymic health had about a 50% lower risk of death. They were significantly less likely to develop lung cancer and had markedly lower cardiovascular mortality. These are not small effects. Importantly, they persist even after accounting for age, sex, smoking, and comorbidities. Two people can be the same chronological age, yet very different biologically. The thymus appears to be one of the organs shaping that divergence.

In our second study, we asked a different question. If the thymus is central to T cell generation, could its health influence how patients respond to immunotherapy? Most biomarkers today focus on the tumor itself. Important, but incomplete. We wanted to look at the other side of the equation: The Patient. Across a pan-cancer cohort of more than 3,400 patients treated with immune checkpoint inhibitors, we found that thymic health is a strong and consistent predictor of outcomes. Patients with higher thymic health had lower risks of disease progression and death. This was particularly evident in cancers such as lung cancer and melanoma, where immunotherapy is widely used. However, we also observed similar associations in other types of cancer, pointing to a broader, tumor-agnostic signal.

Last but not least, I would like to leave a special word of appreciation and congratulations to my co-first authors, Simon Bernatz, Suraj Pai, and Asbjørn Kjær Attermann, to our supervisors, Hugo Aerts and Nicolai Birkbak, and to all the others involved in this major accomplishment.

#Thymus #HealthyAging #Immunology #PrecisionMedicine #Radiology | 15 comments on LinkedIn

Big news: The thymus may be critical for adult health

What if we missed something fundamental about the immune system?

In two back-to-back papers in #Nature we show that the thymus may play a much larger role in health than expected.

Using AI on CT data from 30,000+ people, we found that the health of the thymus varies strongly between people – and is linked to longevity, disease risk, and response to immunotherapy.

So this “forgotten organ” may actually be a key driver of immune resilience throughout life. The implications of this finding could be significant:
• New therapeutic strategies to preserve or restore thymic function
• A new biomarker for aging and disease risk
• Better prediction of immunotherapy outcomes

👉 More to come - we’ll share deeper dives in the coming days

Mass General Brigham, Harvard University, Harvard Medical School, Maastricht University, Mass General Brigham Research, Nature Portfolio, Nature Magazine

Thymic health in adults: https://lnkd.in/ePyWdTAM 
Thymic health and immunotherapy outcomes: https://lnkd.in/emcmz5iu | 14 comments on LinkedIn

A Content Hub aggregating curated immunology resources, from systemic and mucosal immunity knowledge to clinical and applied immunology (allergy, rheumatology, neurology, biotherapies, laboratory medicine) and societal health concerns (vaccine hesitancy) actualized regularly and offering students, t

📚 𝐔𝐧𝐞 𝐦𝐢𝐬𝐞 𝐚̀ 𝐣𝐨𝐮𝐫 𝐦𝐚𝐣𝐞𝐮𝐫𝐞 𝐬𝐮𝐫 𝐥𝐞 𝐒𝐞𝐩𝐬𝐢𝐬 𝐯𝐢𝐞𝐧𝐭 𝐝𝐞 𝐩𝐚𝐫𝐚𝐢̂𝐭𝐫𝐞 𝐝𝐚𝐧𝐬 The Lancet Group (𝐟𝐞́𝐯𝐫𝐢𝐞𝐫 𝟐𝟎𝟐𝟔) !

🔬 Définition & Diagnostic

Le sepsis reste défini comme une dysfonction d'organe menaçant le pronostic vital secondaire à une réponse de l'hôte dérégulée à l'infection. Le diagnostic demeure un défi : les présentations atypiques sont fréquentes, la bactériologie n'est positive que dans 60-70% des cas, et les faux positifs restent nombreux (embolie pulmonaire, lymphome...).
Pas de biomarqueur parfait à ce jour. ⚠️

💉 𝐏𝐫𝐢𝐬𝐞 𝐞𝐧 𝐜𝐡𝐚𝐫𝐠𝐞 : 𝐜𝐞 𝐪𝐮𝐢 𝐜𝐡𝐚𝐧𝐠𝐞 (𝐨𝐮 𝐬𝐞 𝐜𝐨𝐧𝐟𝐢𝐫𝐦𝐞)

🕐 Antibiotiques → Toujours la seule intervention associée de façon constante à une réduction de mortalité.
En choc septique : dans l'heure. En patient non choqué : jusqu'à 5-6h de délai tolérable si le diagnostic est incertain. Dé-escalade dès que possible. Durée : 5-7 jours suffisent dans la majorité des cas.

💧 Remplissage → Jusqu'à 30 mL/kg en phase initiale, mais réévaluation fréquente indispensable. Le bilan hydrique positif persistant est associé à une surmortalité. Penser à la déplétion active dès stabilisation.

💊 Vasopresseurs → Noradrénaline en première ligne, PAM cible 65-70 mmHg. Approche multimodale : Vasopressine en 2ème ligne + Hydrocortisone faible dose (50 mg x4/j) pour améliorer la réponse vasculaire.

🫁 Ventilation → Protection pulmonaire systématique (Vt ~6 mL/kg, Pplat < 30 cmH₂O). Limiter la sédation profonde. Sevrage précoce pour prévenir l'atrophie musculaire.

🍽️ Nutrition → Ne pas nourrir de façon agressive en phase aiguë ! Démarrer l'entérale dans les 3-4 jours. Éviter le suralimentation.

🔮 Perspectives d'avenir

- Biomarqueurs de phénotypage pour personnaliser les thérapies (notamment les corticoïdes)
- Intelligence Artificielle pour la détection précoce
- Focus croissant sur la récupération post-sepsis : 1/6 patients gardent des séquelles sévères, 1/3 décèdent dans l'année

🌍 Ne pas oublier : 85% du fardeau mondial du sepsis concerne les pays à ressources limitées. L'équité d'accès aux soins reste un impératif éthique majeur.

#Réanimation #Sepsis #MédecineIntensive #Lancet #Formation