Abstract:

Primary Membranous Nephropathy (PMN) is a common chronic glomerular disease, which is characterized by glomerular basement membrane thickening and proteinuria. The core pathological mechanism is immune-mediated glomerular injury. In recent years, with the progress of immunology and molecular biology technology, important progress has been made in the pathogenesis of PMN, especially in the molecular mechanism of immune response. Previous studies have shown that anti-PLA2R antibody, as the core pathogenic factor of PMN, can form antigen-antibody complexes by binding to PLA2R on the podocyte membrane, induce the deposition of immune complexes, and lead to glomerular injury and proteinuria by activating the classical complement pathway. In addition, complement cleavage products, such as C3a and C5a, further exacerbate local inflammation and disrupt podocyte barrier function, ultimately leading to glomerulosclerosis. Immune cells also play an important role in the development of PMN. B cells directly participate in the formation of immune complexes by producing IgG4 antibodies. The Th2 type immune response of T cells promotes the production of pathological antibodies by enhancing the activation of B cells. Other immune cells such as dendritic cells and macrophages participate in the disease through antigen presentation, pro-inflammatory cytokine secretion and tissue damage. In this paper, the molecular mechanism of immune response in PMN is described, aiming to provide solid theoretical support and scientific basis for the prevention and treatment of this disease and future research direction.

Key words: primary membranous nephropathy, immune response, immune complexes, anti-PLA2R antibody, immune cells