Regarding autonomous roles in T cells, we have shown that Bcl-3 regulates plasticity and pathogenicity of autoimmune CD4+ T cells in the T cell transfer-induced model of colitis as well as in experimental autoimmune encephalomyelitis (EAE), where Bcl-3 deficient CD4+ T cells attain a less pathogenic IL-17-producing Th17-like phenotype, instead of the pathogenic, IFN-γ producing Th1-like (ex-Th17) phenotype observed in Bcl-3 sufficient mice [28]. This evidence concerns the gene CD4 and experimental autoimmune encephalomyelitis.