CD86 and experimental autoimmune encephalomyelitis: Administration of the AhR agonist 2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) to mice prevented the development of experimental autoimmune encephalomyelitis through tolerization of dendritic cells after decreasing their expression of CD86 while increasing secretion of anti-inflammatory cytokines such as IL-10 and TGF-β [80].