牛痘病毒 A35R 抑制 MHC Ⅱ类抗原呈递。
Vaccinia virus A35R inhibits MHC class II antigen presentation.
机构信息
Brody School of Medicine at East Carolina University, Department of Microbiology and Immunology, Greenville, NC, USA.
出版信息
Virology. 2010 Feb 5;397(1):176-86. doi: 10.1016/j.virol.2009.11.008. Epub 2009 Dec 2.
Abstract
The Vaccinia virus gene A35R (Copenhagen designation) is highly conserved in mammalian-tropic poxviruses and is an important virulence factor, but its function was unknown. We show herein that A35 does not affect viral infectivity, apoptosis induction, or replication; however, we found that A35 significantly inhibited MHC class II-restricted antigen presentation, immune priming of T lymphocytes, and subsequent chemokine and cytokine synthesis. A35 localized to endosomes and reduced the amount of a model antigenic peptide displayed in the cleft of class II MHC. In addition, A35 decreased VV specific T cell responses in vivo. Thus, this is the first report identifying a function for the A35 protein in virulence as well as the first report identifying a VV gene that inhibits peptide antigen presentation.
摘要
痘苗病毒 A35R 基因（哥本哈根命名）在哺乳动物亲和痘病毒中高度保守，是一个重要的毒力因子，但它的功能未知。本文显示，A35 不影响病毒感染力、凋亡诱导或复制；然而，我们发现 A35 显著抑制 MHC Ⅱ类限制性抗原呈递、T 淋巴细胞免疫启动以及随后的趋化因子和细胞因子合成。A35 定位于内体，并减少了 II 类 MHC 裂隙中显示的模型抗原肽的量。此外，A35 降低了 VV 特异性 T 细胞在体内的反应。因此，这是首次报道 A35 蛋白在毒力中的作用，也是首次报道抑制肽抗原呈递的 VV 基因。
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