Recently, Luo et al. evaluated the functions of B7-H3 in the regulation of Th1, Th2, and Th17 subsets in experimental autoimmune encephalomyelitis, experimental asthma, and collagen-induced arthritis using B7-H3 deficient mouse (B7-H3 KO), it suggested that B7-H3 has function on Th1/Th17 and could enhance IFN-γ and IL-17 production [20, 21]. This evidence concerns the gene IL17A and experimental autoimmune encephalomyelitis.