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EBV induces CNS homing of B cells attracting inflammatory T cells

GSE299939 Homo sapiens Expression profiling by high throughput sequencing; Other 6 samples Submitted 2025/07/07 Platform GPL34281
Summary
Epidemiological data have identified Epstein-Barr virus (EBV) infection as the main environmental risk factor for the central nervous system (CNS) autoimmune disease multiple sclerosis (MS). However, how EBV infection initiates MS pathogenesis remains unclear. We now demonstrate that EBV differentiates oligoclonal B cells into MS-associated T-bet+CXCR3+ B cells that home to the CNS in humanized mice. Effector memory CD8+ T cells and CD4+ TH17 cells co-migrate to the brain of EBV infected humanized mice. T-bet+CXCR3+ B cells are capable of colonizing submeningeal brain regions in the absence of other lymphocytes and attract T cells. Depletion of this T-bet+CXCR3+ B cell subset with Rituximab significantly decreases lymphocyte infiltration into the CNS. Thus, we suggest that symptomatic primary EBV infection generates B cell subsets that gain access to the CNS, attract T cells and thereby initiate MS.
Published in
EBV induces CNS homing of B cells attracting inflammatory T cells
Läderach F, Piteros I, Fennell É et al. · Nature 2025 · PMID 40770101 · doi:10.1038/s41586-025-09378-0
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Also filed as BioProject PRJNA1277578 and SRA study SRP592606. Searching any of these in the dataset finder brings you back here.

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