Pathogenic Role of Age‐Associated B Cells in Autoimmune Disorders and Myasthenia Gravis

ABSTRACT Age‐associated B cell (ABC) is a distinctive B cell subset characterized by CD11c and T‐bet expression that accumulates with aging and in autoimmune conditions. This review summarizes current understanding of ABCs in the immunological function and autoimmune pathogenesis of autoimmune diseases, including myasthenia gravis (MG). ABCs arise when B cells are stimulated via B cell receptors and innate immune receptors (notably TLR7/9), in the presence of cytokines secreted by Th1 cells. ABCs behave as antigen‐presenting cells, secrete inflammatory cytokines, and can differentiate into antibody‐secreting cells. In autoimmune disorders, ABCs are thought to undergo expansion, efficiently present self‐antigens to T cells, generate inflammatory mediators, and contribute to autoantibody production. Contemporary single‐cell transcriptomic investigations of MG patients experiencing myasthenic crisis have identified clonally expanded ABC‐like populations. These cells potentially contribute to MG pathogenesis through multiple mechanisms: enhancing T cell activation, sustaining autoreactive plasma cell development, and producing inflammatory cytokines. The increased number of ABCs in late‐onset MG suggests a link between aging and autoimmunity. Targeting ABC development may be a useful treatment approach for antibody‐mediated autoimmune diseases such as MG. Understanding ABCs helps explain how aging affects autoimmunity.