showed that AhR activation by its endogenous ligand 2- (1′H-in-dole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) led to decreased expression of major histocompatibility complex (MHC) class II and co-stimulatory molecules on splenic DCs and T cells, thus promoting the induction of tolerogenic DCs and FoxP3+ Tregs that suppressed experimental autoimmune encephalomyelitis (185). This evidence concerns the gene AHR and experimental autoimmune encephalomyelitis.