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病毒感染的少突胶质细胞的免疫介导损伤:一种多发性硬化症模型

Immune-mediated injury of virus-infected oligodendrocytes A model of multiple sclerosis.

作者信息

Rodriguez M, Pease L R, David C S

机构信息

Departments of Neurology and Immunology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.

出版信息

Immunol Today. 1986 Dec;7(12):359-63. doi: 10.1016/0167-5699(86)90025-3.

Abstract

The causes of primary demyelination in diseases such as multiple sclerosis are still unknown, but it is possible that immune attack triggered by virus infection may be responsible. Theiler's murine encephalitis is a popular animal model of demyelinating diseases, and in this article Moses Rodriguez and his colleagues describe a hypothetical scheme to explain differential susceptibility of inbred strains to infection. They propose a mechanism by which specific demyelination is produced when immune cells interact with viral antigen and major histocompatibility complex (MHC) antigens.

摘要

在诸如多发性硬化症等疾病中,原发性脱髓鞘的病因仍不清楚,但病毒感染引发的免疫攻击可能是其原因。泰勒氏鼠脑脊髓炎是脱髓鞘疾病常用的动物模型,在本文中,摩西·罗德里格斯及其同事描述了一个假设方案,以解释近交系对感染的不同易感性。他们提出了一种机制,即当免疫细胞与病毒抗原和主要组织相容性复合体(MHC)抗原相互作用时,会产生特异性脱髓鞘。

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