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M-T2:一种具有双重活性的痘病毒肿瘤坏死因子受体同源物。

M-T2: a poxvirus TNF receptor homologue with dual activities.

作者信息

Sedger L, McFadden G

机构信息

Department of Biochemistry, University of Alberta, Edmonton, Canada.

出版信息

Immunol Cell Biol. 1996 Dec;74(6):538-45. doi: 10.1038/icb.1996.87.

DOI:10.1038/icb.1996.87
PMID:8989592
Abstract

Poxviruses are experts at manipulating and evading the host's immune response. They have acquired a number of open reading frames which specifically confer direct anti-immune properties, either by mimicking cytokine receptors and growth factors or by disarming cytokine regulatory cascades. The Myxoma T2 protein (M-T2), a TNF receptor homologue, is secreted from virus infected cells and can bind TNF-alpha with high affinity, and thereby inhibit TNF-alpha-mediated cytotoxicity. M-T2 also acts to inhibit virus-induced lymphocyte apoptosis by an as yet undefined mechanism. As such, T2 constitutes a significant virulence factor for poxviruses, influencing the outcome of infection, both in vitro and in vivo.

摘要

痘病毒擅长操纵和逃避宿主的免疫反应。它们获得了一些开放阅读框,这些开放阅读框通过模拟细胞因子受体和生长因子或解除细胞因子调节级联反应来赋予直接的抗免疫特性。黏液瘤T2蛋白(M-T2)是一种肿瘤坏死因子受体同源物,从病毒感染的细胞中分泌出来,能以高亲和力结合肿瘤坏死因子-α,从而抑制肿瘤坏死因子-α介导的细胞毒性。M-T2还通过一种尚未明确的机制抑制病毒诱导的淋巴细胞凋亡。因此,T2是痘病毒的一个重要毒力因子,在体外和体内都影响感染的结果。

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引用本文的文献

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Poliovirus protein 3A inhibits tumor necrosis factor (TNF)-induced apoptosis by eliminating the TNF receptor from the cell surface.脊髓灰质炎病毒蛋白3A通过从细胞表面清除肿瘤坏死因子(TNF)受体来抑制TNF诱导的细胞凋亡。
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