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Autoreactive B cells are a subpopulation of B lymphocytes that recognize and respond to self-antigens due to defects or escapes in central and peripheral tolerance mechanisms[1][7][8]. In health, these cells are largely eliminated through clonal deletion, anergy, and receptor editing during B cell development in the bone marrow and peripheral tissues[1][7][8]. However, residual autoreactive B cells can persist in the mature B cell compartment and, upon activation, contribute to autoimmune diseases via autoantibody production, proinflammatory cytokine secretion, and autoantigen presentation to T cells[1][5][8]. Autoreactive B cells are implicated as disease drivers in conditions such as systemic lupus erythematosus, rheumatoid arthritis, and other autoimmune diseases, where B cell depletion therapies (e.g., anti-CD20 monoclonal antibodies) have proved effective[5][6]. "Autoreactive B cell" is a functional description of an immune cell population rather than a single molecular target, receptor, or protein. It is not a canonical or molecularly defined drug target, but rather a pathogenic cell state that is commonly targeted indirectly by B cell-depleting or -modulating therapies[1][5][6][8].
B cell depletion (anti-CD20 monoclonal antibodies); Inhibition of B cell survival factors (anti-BAFF/Blys)
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