The vitamin D receptor turns off chronically activated T cells.
Ann N Y Acad Sci. 2014 Mar 26. doi: 10.1111/nyas.12408. [Epub ahead of print]
Cantorna MT1, Waddell A.
1Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania; Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania.
T cell proliferation and T helper (TH ) cells that make IL-17 (TH 17 cells) and IFN-γ (TH 1 cells) have been shown to be inhibited by 1,25(OH)2 D3 . Previous work has shown that immune-mediated diseases, where TH 1 and TH 17 cells are pathogenic, are ameliorated with 1,25(OH)2 D3 treatment.
Paradoxically, infectious diseases that require TH 1 and TH 17 responses for host resistance are unaffected by 1,25(OH)2 D3 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 D3 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.
© 2014 New York Academy of Sciences.
KEYWORDS: CD8 T cells, TH17, inflammatory bowel diseases, vitamin D
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