Figure 1.
Model: pathogenesis of IgA vasculitis. The mucosal antigen can activate B-cells in MALT through T-cell-dependent or independent ways. The latter activates B-cells through TLR pathways. With genetic factors, the activated B-cells become plasma cells and produce Gd-IgA1. Gd-IgA1 and anti-Gd-IgA1 autoantibodies form circulating immune complexes together with other components (including sCD89 or complements). Then, the immunocomplex deposit at organs and activate inflammatory responses. In the kidney, the immunocomplex can activate mesangial cells through TfR, leading to the apoptosis of renal cells and recruitment of inflammatory cells. (ADCC, antibody-dependent cytotoxicity; CDC, complement-dependent cytotoxicity; Gd-IgA1, Galactose-deficient IgA1; MAC, membrane attack complex; MALT, Mucosa-associated lymphoid tissue; NET, neutrophil extracellular traps; TfR, transferrin receptor).