AUTOIMMUNITY

L'importance du thymus de plus en plus reconnue.
On est loin d'un organe qui n'avait plus d'importance après la puberté.

A new study coordinated by UMC Utrecht and Amsterdam UMC provides compelling evidence that #longCOVID may be driven by #autoimmunity - where the #immunesystem turns against the body.

▪️ Affecting over 10% of people after #SARSCoV2 #infection, long COVID is known for symptoms like fatigue, pain, and cognitive dysfunction. Yet its underlying #biology has remained unclear.

▪️In this study, researchers transferred IgG #antibodies from long COVID patients into mice triggering persistent pain-like symptoms that lasted weeks. Remarkably, antibodies collected from the same patients two years later produced the same effect, suggesting a long-lasting disease mechanism.

▪️Co-study leads Prof. Niels Eijkelkamp (UMC Utrecht) and Dr. Jeroen den Dunnen (Amsterdam UMC) highlight two key insights:
- Long COVID may be driven by persistent, pathogenic autoantibodies
- The condition is likely heterogeneous, with distinct biological subtypes

▪️The team also identified diverse autoantibodies targeting immune, neurological, and metabolic pathways - many persisting for years.

▪️These findings, published in Cell Reports Medicine by Cell Press, not only strengthen the case for an autoimmune basis of long COVID but also open the door to targeted treatments like immunoadsorption, plasmapheresis, and precision immunotherapy.

As research converges globally on similar findings, this marks a major step toward understanding - and treating - long COVID.

🗃️ See comments for reference.

🔬 Histamine, mélanocytes et vitiligo : et si le chaînon manquant était oxydatif ?
Le vitiligo est encore trop souvent présenté comme une maladie exclusivement auto-immune.
Pourtant, les données accumulées depuis plusieurs années dessinent une lecture plus intégrée, où stress oxydatif, neuro-inflammation et biologie de l’histamine jouent un rôle central.

🧬 Le mélanocyte : une cellule particulièrement vulnérable
Le mélanocyte est une cellule à haute activité métabolique, exposée en permanence à des espèces réactives de l’oxygène (ROS), notamment via la mélanogenèse. Sa survie dépend étroitement de l’équilibre redox local.

🧠 L’histamine : bien plus qu’un médiateur allergique
Dans la peau, l’histamine est libérée par les mastocytes, mais aussi modulée par les kératinocytes, les fibres nerveuses et l’immunité innée.
Elle agit comme un amplificateur inflammatoire et oxydatif, en particulier via l’activation des enzymes DUOX, productrices de peroxyde d’hydrogène (H₂O₂) et sa propre dégradation (DAO en extracellulaire, MAO-B en intracellulaire), qui génère elle aussi du H₂O₂.

Un paradoxe peu discuté
Même lorsque l’histamine est “correctement” dégradée, elle augmente la charge oxydative locale. Si les systèmes antioxydants, notamment glutathion et catalase sont insuffisants, le résultat est une accumulation de H₂O₂ toxique pour le mélanocyte.
🔁 Une boucle auto-entretenue
Histamine ↑ → ROS ↑ → stress oxydatif → souffrance mélanocytaire → signaux de danger → activation immunitaire → mastocytes → histamine ↑

🎯 Implication clinique majeure
Le vitiligo peut être relu comme une pathologie de déséquilibre histamino-oxydatif local, où l’auto-immunité apparaît souvent comme une conséquence plus que comme le point de départ.

👉 Cette approche ouvre des pistes complémentaires comme la réduction de la charge histaminique, la protection antioxydante ciblée, la modulation mastocytaire et la prise en compte du terrain neuro-immun et métabolique.
🔍 Changer de prisme, c’est parfois changer le pronostic.
Dr Lucie WETCHOKO
Source de réflexion:
1- constats de consultation
2- Rôle de l'histamine comme médiateur toxique dans la pathogenèse du vitiligo: 10.4103/0019-5154.119947

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.

Autoimmunity, decoded at single-cell resolution: toward mechanism-driven therapies and smarter diagnostics

Autoimmune diseases are often treated as distinct clinical entities, yet patients experience overlapping biology, variable responses to therapy, and chronic immune dysregulation. This new large-scale single-cell study delivers one of the clearest views yet into what is shared versus truly disease-specific across autoimmunity and why that distinction matters for drug development and patients.

By integrating over 1.3 million immune cells across six autoimmune diseases, the authors move beyond descriptive atlases to identify conserved, mechanistic immune programs that cut across diagnoses, alongside disease-selective features that may explain heterogeneity in outcomes and therapeutic response.

Key findings:
◾ A pan-autoimmune cytotoxic CD8 T cell program marked by clonal expansion and enhanced effector function is observed across multiple diseases, pointing to a shared axis of tissue damage driven by antigen-experienced T cells.

◾ CD14+ monocytes emerge as central orchestrators of humoral autoimmunity, promoting plasma cell survival through elevated TNFSF13B (BAFF) signaling, a pathway already clinically validated but now placed in a broader cross-disease cellular context.

◾ Systematic gene-cluster analysis disentangles cell-intrinsic programs from disease-driven transcriptional states, offering a roadmap for biomarker discovery that is more robust than single-gene approaches.

◾ A machine-learning classifier trained on these single-cell signatures achieves high accuracy in distinguishing autoimmune diseases, highlighting the diagnostic potential of immune-state–based classification rather than symptom-based labels.

This work reinforces a shift underway in immunology and therapeutics: diseases may differ at the organ level, but pathogenic immune circuits are often conserved. Targeting these shared circuits, such as cytotoxic CD8 T cell differentiation or monocyte-plasma cell crosstalk, could enable platform therapies spanning multiple indications, while disease-specific modifiers guide patient stratification and combination strategies.

Equally important, the study highlights how single-cell and AI-enabled frameworks can bridge discovery and clinic, enabling earlier mechanism-based diagnosis, smarter trial design, and clearer go/no-go decisions in immunology pipelines.

The challenge now is translation: validating which of these conserved programs are causal, druggable, and safely modulated in patients. Studies like this provide the systems-level blueprint needed to move autoimmune drug development from reactive suppression toward precise immune reprogramming.

Read the full article here: https://lnkd.in/eJFTRpBt

#AutoimmuneDisease #SingleCellGenomics #Immunology #DrugDevelopment #TranslationalScience

The NEJM has just released the usual end-of-the-year list of most influential papers of 2025.

I found particularly amazing the paper and the editorial concerning allogeneic transplantation of CRISPR genetically-modified Beta cells for type 1 diabetes. A groundbreaking clinical observation that could revolutionise completely this deadly disease. More to come in 2026!

You can download it for free.

Autoantibody-triggered podocyte membrane budding drives autoimmune kidney disease

- Chronic kidney disease affects 1 in 10 people worldwide, with damage to specialized blood filter cells of the kidney, called podocytes, playing a critical role.

- In membranous nephropathy (MN), a major cause of nephrotic syndrome, circulating autoantibodies attack proteins on podocyte foot processes (FPs), damaging the kidney’s filtration barrier.

- This study shows that these autoantibodies trigger the formation of antigen-autoantibody aggregates on the podocyte FP plasma membrane.

- These aggregates bud off as stalked vesicles, termed autoimmunoglobulin-triggered extracellular vesicles (AIT-EVs), which are released into the urine.

- AIT-EVs carry disease-causing autoantibodies, their target antigens, essential FP proteins, and disease-associated stressors representing a mechanism for removing immune complexes (ICs) and waste. However, their excessive release leads to podocyte dysfunction and injury.

- The discovery of AIT-EVs bridges the gap between circulating autoantibodies and podocyte responses and can be harnessed in MN patients.

- Clinically, analysis of urinary AIT-EVs represents a novel non-invasive diagnostic tool to sensitively detect and monitor renal autoimmune activity in patients.

https://lnkd.in/ePD3_xDA

#autoimmunity #kidney #kidneydisease #biomarkers

Vitiligo is an acquired autoimmune depigmenting disorder that affects approximately 0.36% of the global population and presents in three forms based on lesion distribution: non-segmental, segmental and mixed vitiligo. Beyond its visible impact on the skin, vitiligo deeply affects mental well-being and quality of life. The pathogenesis of non-segmental vitiligo is influenced by genetic polymorphisms that are linked to immune response and melanogenesis pathways, whereas environmental factors contribute to disease onset. Diagnosis is generally clinical, with laboratory tests or biopsies rarely required. Melanocyte loss involves mechanisms, such as cellular stress, innate immune activation and adaptive immune responses, that specifically target melanocytes, with a central role for tissue-resident memory T cells. This cascade ultimately leads to the depletion of epidermal melanocytes and impairs melanocyte stem cell regeneration. Clinical management emphasizes shared decision-making with three primary objectives: halting depigmentation, initiating repigmentation and sustaining pigment restoration. Signs of active disease help clinicians to identify patients in need of intervention. Treatments approved in the past 2 years offer potential for reversing disease progression, and emerging therapies targeting key pathways to modulate immune activation and stimulate melanocyte regeneration and differentiation are being tested in clinical trials. Vitiligo is a chronic, autoimmune, depigmenting disorder that has both physiological and psychological effects on affected individuals. In this Primer, Seneschal and colleagues provide an overview of the epidemiology, pathogenesis, diagnosis and management of the condition as well as of its effect on quality of life, and highlight current and emerging treatments.

Read the Review now➡️
Anti-ADAMTS13 Autoantibodies in Immune-Mediated Thrombotic Thrombocytopenic Purpura
By Michael R. Snyder and Robert W. Maitta
Cited 3 times | Viewed 3406 times
Th

Encouraging to see the rapidly evolving translational landscape of CAR-T cell therapy in autoimmune diseases highlighted in Nature. The field is progressing from first-in-human studies in lupus toward phase I/II trials in rheumatoid arthritis, systemic sclerosis, and myositis - including our ongoing efforts at Charité. These developments point toward a potential shift from continuous immunosuppression to time-limited immune reset with the prospect of sustained, treatment-free remission.

Nature: “They don’t have symptoms”: CAR-T therapies send autoimmune diseases into remission
https://lnkd.in/dc2QEThC #AutoimmuneDiseases #Rheumatology #TranslationalMedicine #Immunotherapy

Interested in the Methodology of the 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria?

The Publication Series is Below:

Phase I/II Report: Generation and Reduction of Candidate Criteria (2021) - https://lnkd.in/eM_cbsME

Phase III-A/B Report: Defining and Structuring the Clinical and Laboratory Domains (2025) - https://lnkd.in/euGN5uFd

Phase III-C Report: Assessment of Patient Scenarios (Derivation Cohort) and Refinement of Definitions (2025) - https://lnkd.in/ezt258mf

Phase III-D Report: Multicriteria Decision Analysis (2024) - https://lnkd.in/eabvQvmN

The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria (main paper, which includes the final criteria and phase IV validation report [2023]) - https://lnkd.in/eXnYY72D

Efforts to Better Characterize "Antiphospholipid Antibody Nephropathy" for the 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria: Renal Pathology Subcommittee Report (2024) - https://lnkd.in/epbMZXvS

Medha Barbhaiya Stéphane ZUILY

Thank you to all the contributors.

New research suggests that amyotrophic lateral sclerosis, or ALS, may be partly an autoimmune disease. Scientists discovered that inflammatory immune cells called CD4+ T cells in people with ALS mistakenly attack a protein found in neurons, known as C9orf72. This self-directed immune response appears to drive rapid disease progression, explaining why ALS can destroy motor neurons quickly and lead to severe physical decline.

The study also revealed two distinct patient groups. One group had highly inflammatory CD4+ T cells and shorter predicted survival, while the second group had more anti-inflammatory CD4+ T cells alongside the harmful ones. These protective T cells appear to regulate the immune response, slowing disease progression and allowing some patients to live significantly longer. Understanding this balance between harmful and protective T cells may help explain why survival in ALS varies dramatically, from just a couple of years to several decades in rare cases.

These findings open the door to potential new treatments that boost protective T cell responses and limit harmful inflammation. Future therapies might harness the immune system to slow ALS progression. The study also has implications for other neurodegenerative diseases, such as Parkinson’s, Huntington’s, and Alzheimer’s, where immune cell involvement may similarly influence disease outcomes.

Research Paper 📄
DOI: 10.1038/s41586-025-09588-6

Interpretable inflammation landscape of circulating immune cells

- Inflammation represents an altered state within the immune system, which can manifest as either a protective or a pathological response. The cellular and molecular mediators of inflammation play pivotal roles in nearly every human disease.

- Although major progress has been made in characterizing inflammation in specific diseases, a global, holistic understanding is still elusive.

- In this study, the authors leveraged advances in single-cell transcriptomics to delineate inflammatory processes of circulating immune cells during infection, immune-mediated inflammatory diseases and cancer.

- A single-cell atlas of more than 6.5 million peripheral blood mononuclear cells from 1,047 patients (56% female, 43% male) and 19 diseases was generated allowing to learn a comprehensive model of inflammation in circulating immune cells.

- Beyond a disease-centered classification, the authors modeled the expression profiles of inflammatory molecules to uncover discriminative genes related to immune cell activation, migration, cytotoxic responses and antigen presentation activities.

- A classifier framework based on peripheral blood mononuclear cells (PBMCs) was generated, demonstrating the potential of circulating immune cells to contribute to precision medicine strategies for patients suffering from acute or chronic inflammation.

- As limitations of this study:
>Most samples derive from individuals of European ancestry, and expanding to ancestrally diverse populations will be essential to capture global immune variability.
>The classifier requires prospective validation in independent, multicenter cohorts to assess robustness and clinical applicability.
> Understanding the relationship between circulating and tissue-resident immune cells remains key for diagnostic translation.

https://lnkd.in/d7bKEg4T

#immunology #scRNA #omics #autoimmunity

More excellent #scicomm from Unbiased Science written by Aimee Pugh Bernard, PhD, Leigh Baxt, and Jess Steier. Learn more about the science behind Lupus and new treatments on the horizon for this autoimmune disease likened to "the wolf within."

Fatty liver disease is not just a liver problem.
It is a whole-body metabolic disease.

A major review by Prof. Norbert Stefan, Hannele Yki-Järvinen and Brent A. Neuschwander-Tetri shows that metabolic dysfunction-associated steatotic liver disease affects nearly 4 in 10 adults worldwide and most people with it do not die from liver failure, but from heart disease and cancer…

Important:

• Fatty liver comes in different types, driven by metabolism, fat distribution, or genetics
• The liver actively worsens blood sugar, cholesterol, and clotting risk
• Weight loss helps many…but not everyone responds the same way
• Some treatments improve liver health even without weight loss

The key message is simple:

One-size-fits-all medicine does not work for fatty liver disease!!!

Prevention, early detection and treatment need to focus on metabolic health across the whole body, not just liver enzymes…

If we treat fatty liver early, we also reduce diabetes, heart attacks and strokes later 🤞🏼

What should come first in routine care: liver screening, metabolic screening or both?

If useful, save, share or add your perspective below.

Read original review in The Lancet Group: https://lnkd.in/g3m4tA3k

#metabolichealth #fattyliver #cardiovascularhealth #prevention #publichealth

🔥Don't miss this #FeaturePaper by Moawiah Naffaa, PhD and Ola A. Al-Ewaidat.

Emerging AI- and Biomarker-Driven Precision Medicine in Autoimmune Rheumatic Diseases: From Diagnostics to Therapeutic Decision-Making


🔗More details: https://brnw.ch/21wY2dx


#OpenAccess #AutoimmuneRheumaticDiseases #ArtificialIntelligence #Biomarkers #DigitalHealth

Almost 40% of patients with fulminant herpes simplex virus hepatitis carry autoantibodies neutralizing type I interferons

🧬 Autoimmunity in the CAR era: from chronic suppression to immune reset
Autoimmune diseases affect close to 10% of the global population, and many patients still rely on life-long, non-selective immunosuppression with incomplete control and high toxicity. ⚠️🌍
A new Blood Reviews article on “CARing about autoimmune disorders” reframes CAR-based cell therapies as tools to actively reset immune tolerance, not just turn immunity “down” forever. 🔁🧠
🎯 Layer 1B-cell directed CAR-T as the backbone
CD19 CAR-T has become the leading strategy, inducing deep B-cell depletion and clinical remissions across SLE, IIM, MS, MG and SSc.🦋💪
BCMA CAR-T targets long-lived plasma cells and persistent autoantibodies in SLE, Sjögren’s syndrome and MG.🧫
Next-wave targets (CD20, CD22, CD70, BAFFR) aim for more selective depletion of pathogenic B- and plasma-cell subsets, with dual CD19/BCMA or CD20/BCMA CARs now in trials across multiple autoimmune indications.🌐📊
🧪 Layer 2 Precision tolerance: CAAR-T and CAR-Tregs
CAAR-T cells use the autoantigen as “bait” to delete only autoantigen-specific B cells (MuSK-CAART, pemphigus and others). 🎯
CAR-Tregs are engineered regulatory T cells that restore organ-specific tolerance without global B-cell ablation, with promising data in preclinical models of MS, T1D and vitiligo. 🧠🩺
Together, these platforms turn CARs into precision tolerance inducers rather than purely cytotoxic weapons.
🤖 Layer 3 – Expanding the cellular toolbox
The review maps an ecosystem of CAR platforms for autoimmunity: CAR-NK cells for off-the-shelf cytotoxicity, CAR-macrophages that rewire inflamed tissues, in vivo CAR-T that programs T cells directly in the patient, and allogeneic CRISPR-edited CAR-T products (such as BMS-986515) designed to avoid GVHD and rejection while achieving rapid, durable B-cell depletion. 🧬🧱
🌎 Trials & equity
Around 100 CAR-T/autoimmunity trials are registered worldwide. China and the US lead the field, while many regions remain under-represented, underscoring the need for global manufacturing and regulatory networks so immune reset is not restricted to a few countries. 🌍🤝
🚀 Take-home
CAR technology is emerging as a platform to recalibrate immune balance in autoimmunity and change the natural history of severe, refractory disease:
CD19 / BCMA / CD20 / CD22 / CD70 / BAFFR-directed CAR-T
CAAR-T for autoantigen-specific B cells
CAR-Tregs for organ-specific tolerance
CAR-NK and CAR-macrophages for innate re-programming
In vivo and allogeneic CAR-T for scalable, off-the-shelf access
From chronic immunosuppression to one-time or few-time immune reset with durable remission that is the horizon now opening for autoimmune patients. 🧬🔥
Doi: 10.1016/j.blre.2025.101354
#AutoimmuneDisease #CART #CAART #CARTreg #CARNK #CARMacrophages #CD19CAR #CD20CAR #CD22CAR #CD70CAR #InVivoCART #AllogeneicCART #ImmuneTolerance #SLE #MS #MyastheniaGravis #SystemicSclerosis #T1D #TranslationalImmunology #CellTherapy

🔍 Maladies auto-immunes : et si tout commençait dans vos intestins ? 🔍

Diabète de type 1, sclérose en plaques, polyarthrite rhumatoïde…

Et si ces maladies n’étaient pas uniquement liées à vos gènes ou à votre environnement, mais aussi à la façon dont votre intestin filtre (ou non) ce que vous mangez, respirez ou ressentez ?

Un concept révolutionnaire, longtemps négligé, bouscule aujourd’hui notre compréhension de l’auto-immunité : l’hyperperméabilité intestinale, aussi connue sous le nom de leaky gut.

🧱 L’intestin, votre première ligne de défense

Votre intestin n’est pas qu’un organe digestif.

C’est une frontière immunitaire stratégique : 70 % de vos cellules immunitaires y résident. Il décide de ce qui entre dans votre corps... ou pas.

Mais face à une vie moderne marquée par :
. une alimentation ultra-transformée,
. le stress chronique,
. les toxines environnementales,
. ou encore les infections persistantes…

Cette barrière se fragilise. Des molécules indésirables pénètrent, semant la confusion dans votre système immunitaire, qui peut alors… se retourner contre vous.

C’est ce dérèglement qui précède souvent l’apparition de nombreuses maladies auto-immunes, comme l’ont révélé plusieurs études scientifiques.

🧬 Zonuline : le messager qui ouvre (trop) les portes

Découverte par le Dr Fasano, la zonuline est une protéine qui module l’ouverture des jonctions serrées de votre intestin.

Quand elle est surproduite, ces jonctions s’ouvrent… trop. Résultat : des fragments alimentaires mal digérés, des toxines et même des bactéries peuvent s’infiltrer.

Ce n’est pas une conséquence de la maladie auto-immune.
C’est souvent un élément déclencheur.

🌱 Peut-on réparer l’intestin… et freiner l’auto-immunité ?

Contrairement à ce qu’on pense souvent, une maladie auto-immune n’est pas toujours irréversible.
Si la perméabilité intestinale en est un déclencheur, restaurer la barrière intestinale peut être une piste thérapeutique puissante.

🎯 Voici les 4 piliers pour agir dès maintenant :

1️⃣ Manger anti-inflammatoire : aliments bruts, riches en polyphénols, oméga 3, fibres, épices (curcuma, gingembre…).
2️⃣ Éliminer les agresseurs : gluten, produits ultra-transformés, sucres raffinés, additifs…
3️⃣ Apaiser le stress : cohérence cardiaque, méditation, sommeil réparateur…
4️⃣ Soutenir la muqueuse : L-glutamine, zinc, quercétine, collagène, probiotiques et prébiotiques sont vos alliés.

💡 Une approche fonctionnelle pour agir à la racine

En santé fonctionnelle, on ne masque pas les symptômes, on cherche les causes. Et souvent, elles résident dans l’interconnexion de vos systèmes internes.

💬 Et vous, avez-vous déjà exploré la piste intestinale pour comprendre vos symptômes auto-immuns ?

#SantéFonctionnelle #MaladieAutoImmune #Microbiote #LeakyGut #HyperPerméabilité

🔒 Disclaimer : Pour tout problème de santé, il est essentiel de consulter votre médecin. | 43 comments on LinkedIn

Epstein-Barr virus–mediated B cell reprogramming may initiate systemic lupus erythematosus

- Epstein-Barr virus (EBV) has been making waves as a candidate driver of diseases like multiple sclerosis and Long Covid. It has also long been linked to systemic lupus erythematosus (SLE), although the “why” behind this link has not been defined.

- Here, the authors provide evidence for a link between EBV infection and disease development using an original EBV sequencing (EBV-seq) approach, which combines EBV transcript detection with single-cell transcriptomics.

- The authors evaluated peripheral blood samples from 11 patients with SLE, finding a mean EBV+ B cell frequency of approximately 25 per 10,000 sequenced B cells. In contrast, EBV+ B cell frequencies ranged from 0 to 3 per 10,000 B cells in 10 healthy controls.

- By combining EBV-seq data with single-cell transcriptomics, the authors demonstrated that these latently infected EBV+ B cells were predominantly CD27+CD21low memory B cells exhibiting up-regulation of genes related to antigen processing and presentation, such as IFI30, TAP2, and PSMB6, a population not observed in EBV+ B cells from healthy controls.

- These EBV-infected B cells with antigen-presenting abilities had the capacity to activate autoreactive helper T cells, setting off a chain reaction where those T cells could activate other autoreactive B cells, including uninfected ones.

- These findings support a model in which extremely rare, but overpotent EBV+ “driver” B cells activate helper T cells, which then expand autoreactive EBV− B cells capable of generating the characteristic autoantibodies associated with SLE.

https://lnkd.in/eFGMi75V
https://lnkd.in/ew2DsivE

#lupus #immunology #autoimmunity #rheumatology