Because we recently demonstrated that T cell-independent B cell activation induces immunosuppressive sialylated IgG Abs in vivo (30), we wondered whether the introduction of the 56R allele into lupus-prone Fcgr2b−/− mice may lead to T cell-independent IgG autoAbs and provide a disease-protective effect. The gene discussed is FCGR2B; the disease is systemic lupus erythematosus.