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[感染与多发性硬化症]

[Infection and multiple sclerosis].

作者信息

Yamamura T

机构信息

Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP.

出版信息

Rinsho Shinkeigaku. 1999 Jan;39(1):24-5.

Abstract

Multiple sclerosis is a putative autoimmune disease in which limited numbers of autoimmune T cells reactive to myelin basic protein or proteolipid protein would play critical roles in initiation or augmentation of the inflammatory processes. Owing to the recent immunological studies, it is now possible to discuss the possible link between infectious agents and the development of MS on the molecular terms. This article deals with key issues in this subject such as molecular mimicry between autoantigen and viral peptide, autoimmune T cell stimulation by bacterial superantigens, and regulatory network in MS. In addition to reviewing the current activity in other laboratories, I point out that there might be much more broader range of peptide ligands for autodestructive T cells causing MS. This postulate is based on our recent discovery for the presence of degenerate autoimmune T cells in animal model of MS (EAE). I also indicate the possibility that immune regulatory system could be destroyed by some infectious agents. These informations should have significant implications for management of MS patients.

摘要

多发性硬化症是一种假定的自身免疫性疾病,在该疾病中,数量有限的对髓鞘碱性蛋白或蛋白脂蛋白有反应的自身免疫性T细胞在炎症过程的起始或加剧方面发挥关键作用。由于最近的免疫学研究,现在有可能从分子层面讨论感染因子与多发性硬化症发展之间的可能联系。本文探讨了该主题的关键问题,如自身抗原与病毒肽之间的分子模拟、细菌超抗原对自身免疫性T细胞的刺激以及多发性硬化症中的调节网络。除了回顾其他实验室的当前研究进展外,我指出,导致多发性硬化症的自毁性T细胞可能存在更广泛的肽配体范围。这一假设基于我们最近在多发性硬化症动物模型(实验性自身免疫性脑脊髓炎)中发现的简并性自身免疫性T细胞。我还指出,免疫调节系统可能会被某些感染因子破坏。这些信息对多发性硬化症患者的管理应该具有重要意义。

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