Abstract:

Podocytes,as vital constituents of glomerular filtration barrier,are highly specialized,terminally differentiated cells.Studies on podocyte dysfunction in proteinuric kidney disease have demonstrated that a broad range of stress stimuli can induce podocytes to acquire features of immune cell,including a capacity for phagocytosis and antigen processing and presentation through the formation of peptidemajor histocompatibility complex (MHC) complexes,which ultimately trigger T cell activation and podocyte damage.Podocyte damage resulting from antigen processing and presentation can lead to proteinuria,might be the potential pathogenesis of many forms of human and experimental glomeular disease,such as minimal change disease,focal segmental glomerulosclerosis (FSGS),membranous nephropathy,diabetic nephropathy and lupus nephritis.The discovery of these podocyte functions,which go beyond the role of podocytes in glomeular filtration,has created opportunities for the identification of  novel therapeutic targets for the podocytopathies.From then,a considerable number of studies have investigated the potential of B71 as a therapeutic target and results from the initial clinical trail has proven the feasibility of B71 blockade via CTLA4Ig in patients with recurrent FSGS.However,there are many questions and contradictory findings on the existence and value of podocyte B71 expression in podocytopathies.Thus,there is an urgent need for welldesigned experiment and clinical trails to investigate the robust of B71 expression and B71 blockage therapies in future.

Key words: podocytes, antigen processing and presentation, B7-1, podocytopathies, CTLA4-Ig