This figure illustrates the main topics of and interactions between the projects of section B of CRC 1192. Projects B1-3, B5 and B8 will focus on the pathophysiological mechanisms of podocyte injury in proteinuric GNs (membranous nephropathy, minimal change GN and FSGS) and elucidate the pathogenic role of autoantibodies or a potential circulating factor on the structural and functional level. Projects B3, B5, B6 and B10 will address general mechanisms of podocyte injury mediated by the proteasome, autoantibodies and the complement systems. Moreover, B5 will test the role of nanobodies as a novel class of biologics to target autoantibodies in different forms of GN. Project B6 is aimed at better characterizing complement-mediated glomerulopathies. Project B8 is designed to better understand how immune cell-derived factors promote podocyte injury in pFSGS and Project B9 will investigate the interaction of parietal cells and the immune system in GN with a special focus on glomerular crescents. B10 will decipher the potential role of proteolysis in the control of inflammatory glomerular disease (Illustration: www.hegasy.de).