Unlike IL-12, the subunits of which (IL-12p40 and IL-12p35) are primarily expressed by myeloid-derived APCs, the subunits of IL-35 (Ebi3 and IL-12p35) are expressed by APCs as well as regulatory lymphocyte subsets, signaling in the autocrine fashion described above, suppressing the T cell responses and cytokines that are pathogenic in the context of IBD and numerous other autoimmune disease models, including experimental autoimmune encephalomyelitis (EAE) (14). The gene discussed is EBI3; the disease is experimental autoimmune encephalomyelitis.