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维生素 D、不变自然杀伤 T 细胞与实验性自身免疫病。

Vitamin D, invariant natural killer T-cells and experimental autoimmune disease.

机构信息

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

出版信息

Proc Nutr Soc. 2012 Feb;71(1):62-6. doi: 10.1017/S0029665111003193.

DOI:10.1017/S0029665111003193
PMID:21996367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3733090/
Abstract

Vitamin D is an important regulator of the immune system in general and multiple sclerosis in particular. Experimentally (i), invariant natural killer T (iNKT) cells have been shown to be important suppressors of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE; an animal model of multiple sclerosis). Conversely, in experimental allergic asthma iNKT cells are required for disease induction and are therefore pathogenic. The active form of vitamin D (calcitriol) suppresses EAE. The development of EAE symptoms is accelerated in vitamin D deficiency. Interestingly experimental asthma is less severe in vitamin D deficiency although there is no effect of calcitriol on disease severity. The data suggest that an important target of vitamin D in EAE and asthma are the iNKT cells. Vitamin D and/or vitamin D receptor deficiency results in the impaired development of iNKT cells. Vitamin D is critical very early during development of the immune system. Low levels of vitamin D in utero resulted in significantly reduced numbers of iNKT cells that failed to recover when calcitriol was used to supplement neonatal or adult mice. The data suggest that one of the consequences of early vitamin D deficiency is a reduction in the numbers of iNKT cells that develop. The iNKT cells are required for the beneficial effects of calcitriol in EAE. The important role of vitamin D on iNKT cells could impact the development of human immune-mediated diseases including multiple sclerosis and asthma.

摘要

维生素 D 是免疫系统的重要调节剂,尤其是多发性硬化症。实验表明(i),不变自然杀伤 T(iNKT)细胞是实验性自身免疫性脑脊髓炎(EAE;多发性硬化症的动物模型)等自身免疫性疾病的重要抑制物。相反,在实验性过敏性哮喘中,iNKT 细胞是疾病诱导所必需的,因此具有致病性。维生素 D 的活性形式(骨化三醇)可抑制 EAE。维生素 D 缺乏会加速 EAE 症状的发展。有趣的是,尽管骨化三醇对疾病严重程度没有影响,但维生素 D 缺乏症时实验性哮喘的严重程度较低。这些数据表明,维生素 D 在 EAE 和哮喘中的一个重要靶点是 iNKT 细胞。维生素 D 和/或维生素 D 受体缺乏会导致 iNKT 细胞发育受损。维生素 D 在免疫系统发育的早期至关重要。子宫内维生素 D 水平低会导致 iNKT 细胞数量显著减少,而当用骨化三醇补充新生或成年小鼠时,iNKT 细胞数量无法恢复。这些数据表明,早期维生素 D 缺乏的后果之一是 iNKT 细胞数量减少。iNKT 细胞是骨化三醇在 EAE 中发挥有益作用所必需的。维生素 D 对 iNKT 细胞的重要作用可能会影响包括多发性硬化症和哮喘在内的人类免疫介导性疾病的发展。

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本文引用的文献

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CD1d-restricted iNKT cells, the 'Swiss-Army knife' of the immune system.CD1d 限制性不变自然杀伤 T 细胞,免疫系统的“瑞士军刀”。
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