This notion is supported by previous work in a passive lupus serum transfer nephritis model, which is FcγR-dependent and immune complex-mediated, showing that loss of CD11b facilitates glomerulonephritis via enhanced neutrophil vascular rolling and adhesion (41), indicating that CD11b may in fact regulate leukocyte trafficking under these conditions. Here, FCGR2A is linked to glomerulonephritis.