B-cell activating factor and A proliferation-inducing ligand (BAFF and APRIL)

BAFF (B-cell activating factor, also known as BLyS/TNFSF13B) and APRIL (A proliferation-inducing ligand, TNFSF13) are members of the tumor necrosis factor (TNF) ligand family and critical regulators of both normal and pathological B cell survival, differentiation, and antibody production[1][2][3][5][7][9][10]. They act via three main receptors—BAFF receptor (BAFF-R/TNFRSF13C), transmembrane activator and cyclophilin ligand interactor (TACI/TNFRSF13B), and B cell maturation antigen (BCMA/TNFRSF17)[1][4][9]. BAFF and APRIL are mainly produced by myeloid cells and upregulated by inflammatory cytokines[5]. BAFF and APRIL are implicated in the development of autoimmunity (e.g., SLE, IgA nephropathy) via sustained survival and differentiation of autoreactive B cells and plasma cells[2][3][10], as well as in certain B cell cancers[7][10]. Targeted therapies (e.g., belimumab, atacicept) seek to reduce pathological autoantibody production by blocking BAFF/APRIL signaling. Therapeutic challenges include balancing immune suppression and infection risk while maintaining efficacy[2][10].

Other names

B lymphocyte stimulatorBLySTNFSF13BCD257Tumor necrosis factor ligand superfamily member 13TNFSF13CD256

Blockade of ligand-receptor binding to inhibit B cell survival/differentiation. Neutralization of BAFF and/or APRIL to reduce antibody production and autoimmunity. Receptor decoy to sequester cytokines.