This review demonstrates how BAFF influences autoimmune kidney diseases such as lupus nephritis, suggesting novel therapeutic targets.
Autoimmune kidney diseases usually arise from autoimmune system dysfunction and are characterized by production of autoantibodies. Several autoimmune kidney diseases are currently recognized, including lupus nephritis, antineutrophil cytoplasmic antibody-associated vasculitis, membranous nephropathy, IgA nephropathy. B-cell activating factor (BAFF), a member of the tumor necrosis factor family, serves as a critical regulator of humoral immunity. By binding to specific receptors on the surface of B cells, BAFF regulates their survival, proliferation, differentiation and antibody production, thereby playing a key role in the pathogenesis of autoimmune kidney diseases. Elevated serum BAFF levels, reported across multiple autoimmune diseases, promote aberrant B cell activation and autoantibody production. This review systematically illustrates the biology and immunology of BAFF, and further explores the role of BAFF in those autoimmune kidney diseases, aiming to provide a comprehensive insight into the BAFF molecule.
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Wu et al. (2025) studied this question.
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