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CD25-eBrg is an experimental engineered regulatory B cell (eBreg) therapy designed to treat autoimmune diseases, particularly multiple sclerosis (MS). Developed by researchers at Seattle Children's Research Institute and the University of Washington, these B cells are modified using CRISPR/Cas9 and AAV-mediated homology-directed repair to constitutively express a regulatory cargo—the interleukin-2 receptor alpha chain (CD25)—alongside a B cell receptor (BCR) specific for myelin oligodendrocyte glycoprotein (MOG). Additionally, the cells are engineered to be deficient in Blimp1 (PRDM1) to prevent their differentiation into antibody-secreting plasma cells, allowing them to function as "decoy" B cells that outcompete endogenous B cells for T cell help. In preclinical models of neuroinflammation (EAE), CD25-eBrg cells have demonstrated the ability to suppress pathogenic Th1 CD4+ T cell activation and reduce the secretion of inflammatory cytokines such as IFN-γ and TNF-α, thereby promoting immune tolerance and potentially facilitating CNS repair.
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