期刊
JOURNAL OF IMMUNOLOGY
卷 198, 期 3, 页码 1164-1171出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1601213
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资金
- National Institutes of Health/National Institute of Neurological Disorders and Stroke [NS067563]
- National Center for Complementary and Alternative Medicine
- Office of Dietary Supplements Grant [AT005378]
Vitamin D deficiency is associated with the development of asthma and allergy. The active form of vitamin D [1,25(OH)(2)D] regulates B cells in vitro and mice without the vitamin D receptor (VDR knockout MOB have high serum IgE. Whole-body VDR KO, T cell specific VDR (T-VDR) KO, B cell specific VDR (B-VDR) KO, and vitamin D deficient mice were used to determine the targets of vitamin D in the regulation of IgE in vivo. Vitamin D deficient, VDR KO, and B-VDR KO mice developed hyper-IgE, whereas T-VDR KO mice did not. The data show that IL-10 secretion by B cells and CD1d expression on IL-10 secreting B cells was lower in VDR KO mice. Mesenteric lymph node cultures from VDR KO and B-VDR KO mice secreted higher IgE ex vivo than wild-type (WT) cultures, and the addition of IL-10 eliminated the difference in IgE production between VDR KO and WT cultures. The increase in IgE in VDR KO mice was 2-fold greater than in the B-VDR KO mice, suggesting that VDR deficiency in non-B cells contributes to hyper-IgE in vivo. Antibiotic depletion of the microbiota raised serum IgE 4-fold in both WT and VDR KO mice. The VDR directly and indirectly regulates IgE production in B cells. Through the VDR, vitamin D is an environmental factor that helps to maintain low serum IgE responses.
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