The vitamin D receptor turns off chronically activated T cells

T cell proliferation and T helper (T H ) cells that make IL‐17 (T H 17 cells) and IFN‐γ (T H 1 cells) have been shown to be inhibited by 1,25(OH) 2 D 3 . Previous work has shown that immune‐mediated diseases, where T H 1 and T H 17 cells are pathogenic, are ameliorated with 1,25(OH) 2 D 3 treatment. Paradoxically, infectious diseases that require T H 1 and T H 17 responses for host resistance are unaffected by 1,25(OH) 2 D 3 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) 2 D 3 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.