In experimental autoimmune encephalomyelitis (EAE), deficiency in indoleamine 2,3-dioxygenase (IDO), an enzyme in tryptophan catabolism, led to exacerbated EAE, while administration of tryptophan downstream metabolites could ameliorate EAE by increasing Tregs and inhibiting Th1 and Th17 cells (30). This evidence concerns the gene IDO2 and experimental autoimmune encephalomyelitis.