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多发性硬化症病毒模型中的轴突病理学与脱髓鞘病变

Axonal pathology and demyelination in viral models of multiple sclerosis.

作者信息

Libbey Jane E, Lane Thomas E, Fujinami Robert S

机构信息

Department of Pathology, University of Utah, 15 North Medical Drive East, 2600A EEJMRB, Salt Lake City, UT 84112, USA.

出版信息

Discov Med. 2014 Jul-Aug;18(97):79-89.

Abstract

Multiple sclerosis (MS) is an immune-mediated inflammatory demyelinating disease of the central nervous system (CNS). Monozygotic twin studies suggest that while there is a genetic contribution, genetics alone cannot be the sole determining factor in the development of MS. As the rates of MS are increasing, particularly among women, environmental factors such as viral infections are coming to the foreground as potential agents in triggering disease in genetically susceptible individuals. This review highlights pathological aspects related to two pre-clinical viral models for MS; data are consistent between these two models as experimental infection of susceptible mice can induce axonal degeneration associated with demyelination. These data are consistent with observations in MS that axonal damage or Wallerian degeneration is occurring within the CNS contributing to the disability and disease severity. Such early damage, where axonal damage is primary to secondary demyelination, could set the stage for more extensive immune mediated demyelination arising later.

摘要

多发性硬化症(MS)是一种中枢神经系统(CNS)的免疫介导性炎性脱髓鞘疾病。同卵双胞胎研究表明,虽然存在遗传因素,但仅靠遗传学不能成为MS发病的唯一决定因素。随着MS发病率的上升,尤其是在女性中,诸如病毒感染等环境因素作为在遗传易感性个体中引发疾病的潜在因素正日益凸显。本综述重点介绍了与MS的两种临床前病毒模型相关的病理学方面;这两种模型的数据是一致的,因为易感小鼠的实验性感染可诱导与脱髓鞘相关的轴突变性。这些数据与MS中的观察结果一致,即在CNS内发生轴突损伤或华勒氏变性会导致残疾和疾病严重程度增加。这种早期损伤,即轴突损伤先于继发性脱髓鞘,可能为随后发生更广泛的免疫介导性脱髓鞘奠定基础。

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