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病毒诱导的脱髓鞘和髓鞘再生机制。

Mechanisms of virus-induced demyelination and remyelination.

作者信息

Rodriguez M

机构信息

Department of Neurology and Immunology, Mayo Clinic and Research Foundation, Rochester, Minnesota.

出版信息

Ann N Y Acad Sci. 1988;540(1):240-51. doi: 10.1111/j.1749-6632.1988.tb27066.x.

Abstract

Viral models of demyelination and remyelination provide important clues to the pathogenesis of multiple sclerosis. Determining the precise viral polypeptides recognized by T cells during the demyelinating process will be important in understanding the mechanisms of viral-induced myelin destruction. Isolation, purification, and characterization of factors that promote remyelination and proliferation of oligodendrocytes may provide hope in the treatment of patients with chronic demyelinating disorders.

摘要

脱髓鞘和髓鞘再生的病毒模型为多发性硬化症的发病机制提供了重要线索。确定在脱髓鞘过程中T细胞识别的精确病毒多肽对于理解病毒诱导的髓鞘破坏机制至关重要。分离、纯化和鉴定促进少突胶质细胞髓鞘再生和增殖的因子可能为慢性脱髓鞘疾病患者的治疗带来希望。

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引用本文的文献

本文引用的文献

1
Immune-mediated injury of virus-infected oligodendrocytes A model of multiple sclerosis.
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Science. 1934 Aug 3;80(2066):122. doi: 10.1126/science.80.2066.122-a.
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