The vitamin D receptor turns off chronically activated T cells

Ann N Y Acad Sci. 2014 May;1317:70-5. doi: 10.1111/nyas.12408. Epub 2014 Mar 26.

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.

Keywords: CD8 T cells; TH17; inflammatory bowel diseases; vitamin D.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcitriol / physiology
  • Humans
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / metabolism
  • Lymphocyte Activation
  • Receptors, Calcitriol / physiology*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*

Substances

  • Receptors, Calcitriol
  • Calcitriol