Because our in vitro studies demonstrated that polyclonal IgM inhibited T cell proliferation and differentiation into Th-1 and Th-17 cells (Figures 6B–D) and can also counter pathogenic IgG autoantibodies (as previously discussed), we performed studies to determine whether IgM could inhibit autoimmune insulitis that results in islet cell destruction and diabetes mellitus (DM) in NOD mice (182). The gene discussed is CD40LG; the disease is diabetes mellitus.