In our review out in @MyeloidC14405, we discuss that neuromyeloid effects depend on tissue, cell identity, receptor subtype and signal dynamics. The field needs standardized reporting, stronger causal evidence and better translation to human biology. https://t.co/z4wAEBZWOG #ANS
Nouvelle année, nouvelles résolutions ! 🎉
Voici notre concours spécial résolutions 2026 :
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Résolution n°1 : Prendre soin de son intérieur :
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TAS le 8/01🍀
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https://t.co/rJMF9mcivk
💡Exciting news! Our latest study, in collaboration with Prof. Mirela Kuka’s lab, is out now—uncovering how T cell–derived IFN-γ can suppress T follicular helper (TFH) cells and limit antibody responses. 🚀🧵(1/10) https://t.co/OA0TCnmF7R
🔬Approach: We used a subcutaneous LCMV infection model, tracking virus-specific CD4⁺ T cells. Surprisingly, we found two T-bet⁺ subsets—one producing granzyme B (GzmB) and another expressing Tcf-1, the latter being a TFHprecursor. (2/10)
🌟Key Finding: IFN-γ from T cells drives the TH1 fate and blocks TFHmaturation. When we blocked IFN-γ early, Tcf-1⁺ “precursor” cells fully developed into TFH, boosting germinal center B cells and antibody responses. (3/10)
📊Mechanism: Rather than acting solely via an “autocrine loop,” IFN-γ shapes the microenvironment by acting on other immune cells—likely dendritic cells—thereby steering CD4⁺ T cells toward a TH1-dominant response at the expense of TFH. (4/10)
📌Infections & Vaccines: We also tested other settings—like systemic infections or even MPLA-based immunizations—and consistently observed that reducing IFN-γ can enhance TFH and humoral immunity. Timing is critical for optimal effect. (5/10)
🧬Broader Impact: Our data help explain why some infections trigger robust TH1activity but limited antibody responses, and highlight how precisely timed IFN-γ modulation could improve immunization strategies. (6/10)
🔑Clinical Relevance: In severe or chronic viral infections, TH1-skewed responses can sometimes block high-affinity antibody production. Targeted IFN-γ blockade might tip the balance toward TFH, aiding pathogen clearance or vaccine success. (7/10)
💡Mechanistic Insights: By tuning IFN-γ signals, we can reprogram local lymph nodes and “unlock” TFH potential. This points toward new avenues to combine T cell and B cell–focused therapies for more effective vaccines. (8/10)
👏Huge congratulations to Mirela Kuka, Eleonora Sala, Maria Nelli and all contributors who co-led the study! (9/10)
📖Dive deeper into our research and its implications for antiviral defense and vaccines. We look forward to your thoughts and questions!
Full paper here: https://t.co/OA0TCnmF7R
@SanRaffaeleMI@MyUniSR@ERC_Research@AIRC_it@EMBO@ArmeniseHarvard
(10/10) 💬📚
Metallophilic CD169+ marginal zone macrophages cross-prime CD8+ T cell-mediated protective immunity against blood-borne tumors using a proteasome- and cDC1-independent pathway
@FMauvaisJarvis@pvandenendert@ImmunityCP
https://t.co/oITfIE9Yky
We are hiring! We are looking for a neuro-immunologist for a postdoc position ! Joint project with Professor Sonia Garel on the “United States of Microglia” in Development and Diseases. Please reach out !
Disparition inquiétante | Ling-Diane Zhang, étudiante en 6e année de médecine à Université Paris Cité, a disparu le mardi 16 janvier.
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