期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 3, 页码 1384-1390出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002545
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资金
- National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases [DK070781]
- National Center for Complementary and Alternative Medicine
- Office of Dietary Supplements [AT005378]
Vitamin D status changes with season, but the effect of these changes on immune function is not clear. In this study, we show that in utero vitamin D deficiency in mice results in a significant reduction in invariant NKT (iNKT) cell numbers that could not be corrected by later intervention with vitamin D or 1,25-dihydroxy vitamin D-3 (active form of the vitamin). Furthermore, this was intrinsic to hematopoietic cells, as vitamin D-deficient bone marrow is specifically defective in generating iNKT cells in wild-type recipients. This vitamin D deficiency-induced reduction in iNKT cells is due to increased apoptosis of early iNKT cell precursors in the thymus. Whereas both the vitamin D receptor and vitamin D regulate iNKT cells, the vitamin D receptor is required for both iNKT cell function and number, and vitamin D (the ligand) only controls the number of iNKT cells. Given the importance of proper iNKT cell function in health and disease, this prenatal requirement for vitamin D suggests that in humans, the amount of vitamin D available in the environment during prenatal development may dictate the number of iNKT cells and potential risk of autoimmunity. The Journal of Immunology, 2011, 186: 1384-1390.
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