Fig. 1

Mechanism of action of telitacicept in the treatment of IgAN. Immature B lymphocytes are inappropriately activated by mucosal flora in the mucosal epithelial region. By binding two important cytokines, the B lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), with a B cell activating factor receptor (BAFF-R), the trans-membrane activator and CAML-interactor (TACI), and the B cell maturation antigen (BCMA), the three B lymphocyte-membrane-surface-related receptors, abnormally activate immature B lymphocytes in bone marrow and peripheral lymphoid tissues mature and differentiate. The mature differentiated plasma cells enter the systemic circulation, galactose-deficient IgA1 (Gd-IgA1) secretion increases, anti-galactose-deficient IgA1 (anti-Gd-IgA1) autoantibody secretion increases, and a more immune complex forms. As a biological agent can simultaneously block cytokines BLys and APRIL, it can also prevent their binding to the three B lymphocyte-membrane-surface-related receptors (BAFF-R, TACI, and BCMA). This prevents the maturation of B lymphocytes, thereby preventing the release and development of Gd-IgA1 and anti-Gd-IgA1 antibodies into the bloodstream and preventing the development of immunological complexes in the kidney's mesangial region. Telitacicept is a fusion protein comprising a recombinant trans-membrane activator, calcium modulator, and cyclophilin ligand interactor (TACI) receptor fused to the fragment crystallisable (Fc) domain of human immunoglobulin G (IgG)