Fig. 1: The role model of immune cells in membranous nephropathy.

APCs can recognize PLA2R antigens and then present PLA2R fragments on MHC Class II molecules on their surface to Naïve T. Stimulated T cells differentiate into helper T (Th) cells and release cytokines, which are fed back to B cells, stimulating division and differentiation into plasma cells and antibody-producing and memory B cells. Autoantibodies begin to target PLA2R on the basal surface of podocytes and activate complement to form membrane attack complex (MAC). NK exerts antibody-dependent cell-mediated cytotoxicity (ADCC) by interacting with immune complexes via its Fc receptor. Macrophages cause kidney injury by producing the inflammatory factor TNF-α to promote inflammation. CR1 complement receptor 1, TCR T cell receptor, APCs antigen-presenting cells, NK Natural killer, DC Dendritic cells, GC-B germinal center B, IFN-γ cytokines interferon γ, TNF-α tumor necrosis factor This image was created by Figdraw.