The vitamin D receptor turns off chronically activated T cells.

T cell proliferation and T helper (T_H) cells that make IL-17 (T_H17 cells) and IFN-γ (T_H1 cells) have been shown to be inhibited by 1,25(OH)₂D₃. Previous work has shown that immune-mediated diseases, where T_H1 and T_H17 cells are pathogenic, are ameliorated with 1,25(OH)₂D₃ treatment. Paradoxically, infectious diseases that require T_H1 and T_H17 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]