FCGR2B and arthritic joint disease: Bartsch et al. found that sialylated anti-Col II IgG1 antibodies significantly attenuated Col II-induced arthritis in FcγRIIb-deficient mice, with decreased accumulations of Th17 cells in the popliteal and brachial lymph nodes, in line with the in vitro finding that coculturing bone marrow-derived DCs from FcγRIIb-deficient mice with sialylated ICs inhibited secretion of IL-6, the critical cytokine for Th17 generation 110.