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维生素 D、多发性硬化症和炎症性肠病。

Vitamin D, multiple sclerosis and inflammatory bowel disease.

机构信息

Department of Veterinary and Biomedical Science, The Center for Molecular Immunology and Infectious Disease, 115 Henning Bldg., The Pennsylvania State University, University Park, PA 16802, USA.

出版信息

Arch Biochem Biophys. 2012 Jul 1;523(1):103-6. doi: 10.1016/j.abb.2011.11.001. Epub 2011 Nov 10.

DOI:10.1016/j.abb.2011.11.001
PMID:22085500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3374859/
Abstract

It has now been more than 20years since the vitamin D receptor was identified in cells of the immune system. The immune system has now been established as an important target of vitamin D. Vitamin D receptor knockout and vitamin D deficient mice have a surplus of effector T cells that have been implicated in the pathology of multiple sclerosis (MS) and inflammatory bowel disease (IBD). The active form of vitamin D directly and indirectly suppresses the function of these pathogenic T cells while inducing several regulatory T cells that suppress MS and IBD development. There is reason to believe that vitamin D could be an environmental factor that may play a role in the development of these immune mediated diseases in the clinic but at present there has not been a causal relationship established. Nonetheless, current evidence suggests that improving vitamin D status and/or using vitamin D receptor agonists may be useful in MS and IBD.

摘要

自从免疫系统中的维生素 D 受体被发现以来,已经过去了 20 多年。免疫系统现已被确定为维生素 D 的重要靶标。维生素 D 受体敲除和维生素 D 缺乏的小鼠具有过量的效应 T 细胞,这些细胞与多发性硬化症 (MS) 和炎症性肠病 (IBD) 的病理学有关。维生素 D 的活性形式直接和间接地抑制这些致病性 T 细胞的功能,同时诱导几种调节性 T 细胞,抑制 MS 和 IBD 的发展。有理由相信,维生素 D 可能是一种环境因素,可能在这些免疫介导的疾病的临床发展中发挥作用,但目前尚未建立因果关系。尽管如此,目前的证据表明,改善维生素 D 状况和/或使用维生素 D 受体激动剂可能对 MS 和 IBD 有用。

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本文引用的文献

1
Vitamin D deficiency diminishes the severity and delays onset of experimental autoimmune encephalomyelitis.维生素 D 缺乏会降低实验性自身免疫性脑脊髓炎的严重程度并延迟其发病。
Arch Biochem Biophys. 2011 Sep 15;513(2):140-3. doi: 10.1016/j.abb.2011.07.005. Epub 2011 Jul 19.
2
1,25-dihydroxyvitamin D(3) ameliorates Th17 autoimmunity via transcriptional modulation of interleukin-17A.1,25-二羟维生素 D(3) 通过调节白细胞介素-17A 的转录来改善 Th17 自身免疫。
Mol Cell Biol. 2011 Sep;31(17):3653-69. doi: 10.1128/MCB.05020-11. Epub 2011 Jul 11.
3
Vitamin D-mediated immune regulation in multiple sclerosis.维生素 D 介导的多发性硬化症中的免疫调节。
J Neurol Sci. 2011 Dec 15;311(1-2):23-31. doi: 10.1016/j.jns.2011.06.027. Epub 2011 Jul 2.
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Converging pathways lead to overproduction of IL-17 in the absence of vitamin D signaling.在缺乏维生素 D 信号的情况下, converge 途径导致 IL-17 的过度产生。
Int Immunol. 2011 Aug;23(8):519-28. doi: 10.1093/intimm/dxr045. Epub 2011 Jun 22.
5
Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease. Epstein-Barr 病毒潜伏期的表观遗传失调与自身免疫性疾病的发生。
Adv Exp Med Biol. 2011;711:82-102. doi: 10.1007/978-1-4419-8216-2_7.
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Experimental models of multiple sclerosis.多发性硬化症的实验模型。
Curr Opin Neurol. 2011 Jun;24(3):291-9. doi: 10.1097/WCO.0b013e328346c226.
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Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis.纬度与多发性硬化症的患病率显著相关:一项荟萃分析。
J Neurol Neurosurg Psychiatry. 2011 Oct;82(10):1132-41. doi: 10.1136/jnnp.2011.240432. Epub 2011 Apr 8.
8
Genetic predisposition to autoimmunity--what have we learned?自身免疫遗传易感性——我们学到了什么?
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1,25-Dihydroxyvitamin D3 acts directly on the T lymphocyte vitamin D receptor to inhibit experimental autoimmune encephalomyelitis.1,25-二羟维生素 D3 通过直接作用于 T 淋巴细胞维生素 D 受体抑制实验性自身免疫性脑脊髓炎。
Eur J Immunol. 2011 Mar;41(3):822-32. doi: 10.1002/eji.201040632. Epub 2011 Feb 1.
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Vitamin D suppresses Th17 cytokine production by inducing C/EBP homologous protein (CHOP) expression.维生素 D 通过诱导 C/EBP 同源蛋白(CHOP)的表达来抑制 Th17 细胞因子的产生。
J Biol Chem. 2010 Dec 10;285(50):38751-5. doi: 10.1074/jbc.C110.185777. Epub 2010 Oct 25.