title: The vitamin D receptor turns off chronically activated T cells.
abstract: 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.
authors.affiliation: Department 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.
authors.forename: Margherita T
authors.initials: MT
authors.lastname: Cantorna
authors.forename: Amanda
authors.initials: A
authors.lastname: Waddell
mesh_terms: D000818:Animals; D002117:Calcitriol / Q000502:physiology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation; D018167:Receptors, Calcitriol / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*
chemical_list: D018167:Receptors, Calcitriol; D002117:Calcitriol
keywords: CD8 T cells; TH17; inflammatory bowel diseases; vitamin D