To further investigate the protective effect of sialylated autoantigen-specific IgG Abs on the development of autoimmune pathology, here we studied the disease course in lupus nephritis-prone FcγRIIB-deficient (Fcgr2b−/−) mice and in 56R+/−Fcgr2b−/− mice that express a transgenic self- and polyreactive B cell receptor (BCR) (43–46) and produce T cell-independent sialylated IgG2a and IgG2b autoAbs (47). Here, FCGR2B is linked to lupus nephritis.