Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms.
Control of Circulating IgE by the Vitamin D Receptor In Vivo Involves B Cell Intrinsic and Extrinsic Mechanisms.
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维生素D受体在体内控制循环IgE涉及B细胞的固有和外在机制。
DOI：
10.4049/jimmunol.1601213
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发表时间：
2017-02-01
期刊：
影响因子：
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通讯作者：
Cantorna MT
中科院分区：
文献类型：
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作者：
James J;Weaver V;Cantorna MT
维生素D缺乏与哮喘和过敏的发展有关。活性形式的维生素D（1，25（OH）2D）在体外调节B细胞，并且没有维生素D受体（VDR KO）的小鼠具有高血清IgE。使用全身VDR KO、T-VDR KO、B-VDR KO和维生素D缺陷小鼠来确定维生素D在体内调节IgE中的靶点。维生素D缺乏、VDR KO和B-VDR KO小鼠出现高IgE，而T-VDR KO小鼠没有。数据显示，在VDR KO小鼠中，B细胞的IL-10分泌和B10细胞上的CD 1d表达较低。来自VDR KO和B-VDR KO小鼠的肠系膜淋巴结培养物比WT培养物离体分泌更高的IgE，并且添加IL-10消除了VDR KO和WT培养物之间IgE产生的差异。VDR KO小鼠中IgE的增加是B-VDR KO小鼠中的2倍，表明非B细胞中的VDR缺陷导致体内高IgE。在WT和VDR KO小鼠中，微生物群的抗生素消耗使血清IgE升高4倍。VDR直接和间接调节B细胞中的IgE产生。维生素D通过VDR是一种环境因素，有助于维持低血清IgE反应。
Vitamin D deficiency is associated with the development of asthma and allergy. The active form of vitamin D (1,25(OH)2D) regulates B cells in vitro and mice without the vitamin D receptor (VDR KO) have high serum IgE. Whole body VDR KO, T-VDR KO, 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, while T-VDR KO mice did not. The data show that IL-10 secretion by B cells and CD1d expression on B10 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 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. Vitamin D, through the VDR, is an environmental factor that helps to maintain low serum IgE responses.