To combine parts of measles with an inflammatory stimulus, would that be a good idea? 😄

New Article! T cell immunomonitoring: a comparative analysis of traditional and novel methods to quantify and characterize human antigen-specific T cells

Congratulations! Shouldn‘t you be writing „Thrilled to announce…“? 😀

Fantastic preprint showing how circulating EBV-specific CD8+ T cells in MS adopt a GZMK+ effector–memory state that is primed to migrate to the CNS & may drive neuroinflammation through non-cytolytic interactions with B cells & myeloid cells. 🧵👇 1/

Dear Redwan, thank you for your kind words! Glad you like it! We saw your study, too, and were very happy to see it is the same subset (CD8+!) depleted after aCD20 treatment. Yours came out just in time so we could still cite it. 🤓

This provides a mechanism linking peripheral EBV immunity to CNS autoimmunity that is complementary to molecular mimicry: infection history may become encoded in long-lived T cell states that later influence tissue-specific inflammatory disease. (7/8)

💡 We therefore propose that EBV can leave a durable imprint on the differentiation state, tissue tropism and function of antiviral T cells. Once these cells enter the CNS, they may contribute to inflammation through a non-canonical mode of B and myeloid cell activation. (6/8)

Functionally, activated CD8⁺ T cells promoted atypical B cell and plasmablast formation, while GZMK-enriched effector-memory cells induced inflammatory IL-6 and IL-8 responses in myeloid cells. (5/8)

🔎 Naturally captured T cell–APC multiplets allowed us to map antigen specificity directly onto cellular interactions. EBV-reactive CD8⁺ T cells preferentially interacted with B lineage cells — rather than behaving simply as classical cytotoxic antiviral cells. (4/8)

We found that CNS accumulation was not random. T cell clones carrying a GZMK⁺ effector-memory program already in peripheral blood were strongly biased toward the CSF. Strikingly, EBV-specific T cells were particularly enriched for this tissue-oriented state. (3/8)

EBV is neccessary yet insufficient for MS. Antibody cross-reactivity has provided an important mechanistic link. What EBV-specific T cells actually do in MS has remained less clear. We generated a single-cell atlas of T cells from paired blood and CSF of newly diagnosed MS and controls. (2/8)