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泰勒氏病毒诱导的脑脊髓炎中少突胶质细胞的持续感染。

Persistent infection of oligodendrocytes in Theiler's virus-induced encephalomyelitis.

作者信息

Rodriguez M, Leibowitz J L, Lampert P W

出版信息

Ann Neurol. 1983 Apr;13(4):426-33. doi: 10.1002/ana.410130409.

Abstract

Mice infected with Theiler's murine encephalomyelitis virus (TMEV) develop a chronic relapsing demyelinating myelitis. To determine the localization of viral antigen in infected cells of the spinal cord, we studied TMEV-infected SJL/J mice using immunoelectron microscopic peroxidase-antiperoxidase techniques. Viral antigens were expressed in the cytoplasm of neurons and astrocytes 4 and 11 days postinfection. At 28 days postinfection, macrophages, astrocytes, and oligodendrocytes showed viral antigen in their cytoplasm. At 45, 83, 270, and 360 days postinfection, most infected cells were oligodendrocytes as revealed ultrastructurally by immunoperoxidase staining of prominent glial loops that connect with myelin lamellae. Some of these sheaths also showed Schmidt-Lanterman incisures that stained for viral antigen. Virus could be recovered at low titers for the duration of the illness. The findings indicate that TMEV induces persistent infection of oligodendrocytes which could then become the target of immune-mediated injury resulting in demyelination.

摘要

感染泰勒氏鼠脑脊髓炎病毒(TMEV)的小鼠会发展出慢性复发性脱髓鞘性脊髓炎。为了确定病毒抗原在脊髓感染细胞中的定位,我们使用免疫电子显微镜过氧化物酶-抗过氧化物酶技术研究了感染TMEV的SJL/J小鼠。病毒抗原在感染后4天和11天在神经元和星形胶质细胞的细胞质中表达。在感染后28天,巨噬细胞、星形胶质细胞和少突胶质细胞在其细胞质中显示出病毒抗原。在感染后45、83、270和360天,通过与髓鞘板层相连的突出胶质环的免疫过氧化物酶染色超微结构显示,大多数感染细胞是少突胶质细胞。其中一些鞘也显示出对病毒抗原染色的施密特-兰特尔曼切迹。在疾病持续期间,可以以低滴度回收病毒。这些发现表明,TMEV诱导少突胶质细胞持续感染,然后少突胶质细胞可能成为免疫介导损伤的靶标,导致脱髓鞘。

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