Figure 1.

Mechanism of BAFF/APRIL-induced autoimmune nephropathy: BAFF and APRIL form soluble trimers following cleavage by furin; through differential binding to BAFF-R, TACI, and BCMA receptors, they regulate B-cell survival, maturation, and differentiation. Concurrently, BAFF can directly activate CD4⁺ T cells, promote Tfh differentiation, and upregulate the Th1/Th2 and Th17/Treg ratios, thereby further enhancing the survival, differentiation, and antibody production of autoreactive B cells. It is involved in the pathogenesis of immune complex-associated nephropathies such as IgA nephropathy, lupus nephritis, and primary membranous nephropathy. Created with BioRender.