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中枢神经系统炎性脱髓鞘中免疫耐受的机制。

Mechanisms of immunological tolerance in central nervous system inflammatory demyelination.

作者信息

Mari Elisabeth R, Moore Jason N, Zhang Guang-Xian, Rostami Abdolmohamad

机构信息

Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

出版信息

Clin Exp Neuroimmunol. 2015 Aug 1;6(3):264-274. doi: 10.1111/cen3.12196. Epub 2015 Mar 22.

Abstract

Multiple sclerosis is a complex autoimmune disease of the central nervous system that results in a disruption of the balance between pro-inflammatory and anti-inflammatory signals in the immune system. Given that central nervous system inflammation can be suppressed by various immunological tolerance mechanisms, immune tolerance has become a focus of research in the attempt to induce long-lasting immune suppression of pathogenic T cells. Mechanisms underlying this tolerance induction include induction of regulatory T cell populations, anergy and the induction of tolerogenic antigen-presenting cells. The intravenous administration of encephalitogenic peptides has been shown to suppress experimental autoimmune encephalomyelitis and induce tolerance by promoting the generation of regulatory T cells and inducing apoptosis of pathogenic T cells. Safe and effective methods of inducing long-lasting immune tolerance are essential for the treatment of multiple sclerosis. By exploring tolerogenic mechanisms, new strategies can be devised to strengthen the regulatory, anti-inflammatory cell populations thereby weakening the pathogenic, pro-inflammatory cell populations.

摘要

多发性硬化症是一种中枢神经系统的复杂自身免疫性疾病,会导致免疫系统中促炎信号和抗炎信号之间的平衡被打破。鉴于中枢神经系统炎症可被多种免疫耐受机制抑制,免疫耐受已成为诱导致病性T细胞长期免疫抑制研究的重点。这种耐受诱导的潜在机制包括调节性T细胞群体的诱导、无反应性以及耐受性抗原呈递细胞的诱导。已证明静脉注射致脑炎性肽可通过促进调节性T细胞的生成和诱导致病性T细胞凋亡来抑制实验性自身免疫性脑脊髓炎并诱导耐受。诱导长期免疫耐受的安全有效方法对于多发性硬化症的治疗至关重要。通过探索耐受机制,可以设计新的策略来增强调节性抗炎细胞群体,从而削弱致病性促炎细胞群体。

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