Immune system-mediated cellular and molecular mechanisms in idiopathic membranous nephropathy pathogenesis and possible therapeutic targets.

Idiopathic membranous nephropathy (IMN) has recently attracted much attention due to the development of auto antibodies, anti-phospholipase A2 receptor and anti-thrombospondin type I domain-containing 7A on podocytes, the establishment of immune networks complexes in circulation as well as the development of autoreactive immune cells against kidney, in both innate and adaptive participants. The auto inflammatory responses in IMN leads to the dysfunction of glomerular cells to represent pathological status. T cells, as a crucial factor in the immune network, support B cell-related responses and develop inflammation and cytotoxicity. They have the most determining roles in the autoimmune diseases. Activation of T cells occurs just before their infiltration in kidney. This process is definitely accompanied by costimulatory factors and cytokines, in order to develop and increase the number of these cells. In addition, altered B cell signaling network by the B cell receptor and co receptors such as B cell-activating factor receptor (BAFFR) stimulates the autoimmune-related pathogenesis. Autoantigens exposure and kidney infiltration of naive T cells lead to their local development. Furthermore, losing peripheral immune tolerance towards kidney antigens, will result in IMN. The growing findings about different immune system factors, cells and molecular mechanism have also revealed new pathways of pathogenesis and diagnosis approaches, such as personalized medicine in MN patients. This review aims to discuss the recent findings in adaptive immune cells, and distinguishes between intact and undone researches about pathogenesis and molecular signaling pathways of immune system in MN disease.