IDO1 and experimental autoimmune encephalomyelitis: 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).