The vitamin D receptor turns off chronically activated T cells.

T cell proliferation and T helper (TH) cells that make IL-17 (TH17 cells) and IFN-γ (TH1 cells) have been shown to be inhibited by 1,25(OH)2D3. Previous work has shown that immune-mediated diseases, where TH1 and TH17 cells are pathogenic, are ameliorated with 1,25(OH)2D3 treatment. Paradoxically, infectious diseases that require TH1 and TH17 responses for host resistance are unaffected by 1,25(OH)2D3 treatment. Resting T cells are not responsive to vitamin D because they do not express the vitamin D receptor (VDR) until late after activation. T cells activated following an infection help clear the infection, and since the antigen is eliminated, vitamin D is not needed to dampen the immune response. Conversely, in immune-mediated disease, there is chronic T cell activation, and in this scenario, vitamin D and 1,25(OH)2D3 are critical for inhibiting T cell proliferation and cytokine production. Vitamin D is a late regulator of T cell function and acts to turn off T cells. This paper will review these data. [ABSTRACT FROM AUTHOR]