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一次骨化三醇给药可短暂增加 Helios+FoxP3+T 细胞,并改善自身免疫性脱髓鞘疾病。

One calcitriol dose transiently increases Helios+ FoxP3+ T cells and ameliorates autoimmune demyelinating disease.

机构信息

Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706, United States.

出版信息

J Neuroimmunol. 2013 Oct 15;263(1-2):64-74. doi: 10.1016/j.jneuroim.2013.07.016. Epub 2013 Aug 6.

Abstract

Multiple sclerosis (MS) is an incurable inflammatory demyelinating disease. We investigated one calcitriol dose plus vitamin D3 (calcitriol/+D) as a demyelinating disease treatment in experimental autoimmune encephalomyelitis (EAE). Evidence that calcitriol-vitamin D receptor pathway deficits may promote MS, and data showing calcitriol enhancement of autoimmune T cell apoptosis provided the rationale. Whereas vitamin D3 alone was ineffective, calcitriol/+D transiently increased central nervous system (CNS) Helios(+)FoxP3(+) T cells and sustainably decreased CNS T cells, pathology, and neurological deficits in mice with EAE. Calcitriol/+D, which was more effective than methylprednisolone, has potential for reversing inflammatory demyelinating disease safely and cost-effectively.

摘要

多发性硬化症(MS)是一种无法治愈的炎症性脱髓鞘疾病。我们研究了一种钙三醇加维生素 D3(钙三醇/ + D)作为实验性自身免疫性脑脊髓炎(EAE)的脱髓鞘疾病治疗方法。钙三醇-维生素 D 受体途径缺陷可能促进 MS 的证据,以及钙三醇增强自身免疫性 T 细胞凋亡的数据为这一研究提供了依据。虽然单独使用维生素 D3 无效,但钙三醇/ + D 可短暂增加中枢神经系统(CNS)Helios(+)FoxP3(+)T 细胞,并可持续减少 CNS T 细胞、病理学和 EAE 小鼠的神经功能缺损。钙三醇/ + D 比甲基强的松龙更有效,具有安全有效地逆转炎症性脱髓鞘疾病的潜力。

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