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Background  Vitamin D 3 , the most physiologically relevant form of vitamin D, is an essential organic compound that has been shown to have a crucial effect on the immune responses. Vitamin D 3  ameliorates the onset of the experimental autoimmune encephalomyelitis (EAE); however, the direct effect of vitamin D 3  on T cells is largely unknown.    Methodology/Principal Findings  In an  in vitro  system using cells from mice, the active form of vitamin D 3  (1,25-dihydroxyvitamin D 3 ) suppresses both interleukin (IL)-17-producing T cells (T H 17) and regulatory T cells (Treg) differentiation via a vitamin D receptor signal. The ability of 1,25-dihydroxyvitamin D 3  (1,25(OH) 2 D 3 ) to reduce the amount of IL-2 regulates the generation of Treg cells, but not T H 17 cells. Under T H 17-polarizing conditions, 1,25(OH) 2 D 3  helps to increase the numbers of IL-10-producing T cells, but 1,25(OH) 2 D 3 's negative regulation of T H 17 development is still defined in the IL-10 −/−  T cells. Although the STAT1 signal reciprocally affects the secretion of IL-10 and IL-17, 1,25(OH) 2 D 3  inhibits IL-17 production in STAT1 −/−  T cells. Most interestingly, 1,25(OH) 2 D 3  negatively regulates CCR6 expression which might be essential for T H 17 cells to enter the central nervous system and initiate EAE.    Conclusions/Significance  Our present results in an experimental murine model suggest that 1,25(OH) 2 D 3  can directly regulate T cell differentiation and could be applied in preventive and therapeutic strategies for T H 17-mediated autoimmune diseases.

1,25-Dihydroxyvitamin D3 Inhibits the Differentiation and Migration of TH17 Cells to Protect against Experimental Autoimmune Encephalomyelitis