Recent advances in understanding the multifaceted pathobiology of rheumatoid arthritis have highlighted the pivotal role and continuing crosstalk between activated immune cells, pro-inflammatory cytokines, and matrix-degrading mediators, promoting chronic inflammation as well as irreversible tissue damage within an autoimmune background. B cells are widely recognized as leading players in immune-mediated pathology based on their ability to produce not only different patterns of autoantibodies and driving cytokine synthesis but also as independent antigen-presenting cells and by modulating the specific activation of T cells. Overwhelming evidence emphasized the role of BAFF, a B-cell-activating factor, and BAFF receptors (TACI, BCMA, BAFF-R) in promoting B-cell homeostasis, proliferation, and survival under normal and autoimmune systemic disorders. We systematically reviewed data from literature focusing on BAFF, its homolog molecule APRIL, and BAFF-binding receptors biology, dysregulation of BAFF/BAFF receptor signaling in autoimmune settings, and current status of targeting BAFF/BAFF receptor pathway for rheumatoid arthritis.
Part of the book: New Developments in the Pathogenesis of Rheumatoid Arthritis