Interestingly, based on the murine models of autoimmune diseases, i.e., antibody-mediated K/BxN arthritis and T cell-mediated experimental autoimmune encephalitis, a recent report proposed that induction of interleukin 33 (IL-33) in macrophages by IVIG through interaction of α2,6-sialylated crystallizable fraction (Fc) with SIGN-R1 or human DC-SIGN is essential for the expansion of Treg cells [19, 20]. The gene discussed is IL33; the disease is arthritic joint disease.