A research team from Westlake Laboratory of Life Sciences and Biomedicine published a study in Immunity, elucidating the molecular mechanisms by which meningeal B cells drive neuroinflammatory relapse in multiple sclerosis (MS) through antigen presentation and cognate interactions with T cells. Using the experimental autoimmune encephalomyelitis (EAE) model, combined with single-cell RNA sequencing and immunofluorescence, the study revealed that meningeal autoreactive B cells, activated by MOG antigens, promote T cell-mediated inflammation via MHC-II-mediated antigen presentation, forming a “T-B cell-neutrophil-endothelial cell” inflammatory loop. Targeted depletion of local brain B cells effectively alleviated EAE relapse, offering new directions for MS precision therapy. AtaGenix provided high-purity MOG protein, supporting key experimental validations.
