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NKG2D在自然杀伤细胞介导的抗痘病毒病中的作用。

A role for NKG2D in NK cell-mediated resistance to poxvirus disease.

作者信息

Fang Min, Lanier Lewis L, Sigal Luis J

机构信息

Program of Viral Pathogenesis, Division of Basic Sciences, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America.

出版信息

PLoS Pathog. 2008 Feb 8;4(2):e30. doi: 10.1371/journal.ppat.0040030.

DOI:10.1371/journal.ppat.0040030
PMID:18266471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2233669/
Abstract

Ectromelia virus (ECTV) is an orthopoxvirus (OPV) that causes mousepox, the murine equivalent of human smallpox. C57BL/6 (B6) mice are naturally resistant to mousepox due to the concerted action of innate and adaptive immune responses. Previous studies have shown that natural killer (NK) cells are a component of innate immunity that is essential for the B6 mice resistance to mousepox. However, the mechanism of NK cell-mediated resistance to OPV disease remains undefined. Here we show that B6 mice resistance to mousepox requires the direct cytolytic function of NK cells, as well as their ability to boost the T cell response. Furthermore, we show that the activating receptor NKG2D is required for optimal NK cell-mediated resistance to disease and lethality. Together, our results have important implication towards the understanding of natural resistance to pathogenic viral infections.

摘要

痘苗病毒(ECTV)是一种正痘病毒(OPV),可引起鼠痘,即小鼠的天花。C57BL/6(B6)小鼠由于先天性和适应性免疫反应的协同作用而对鼠痘具有天然抵抗力。先前的研究表明,自然杀伤(NK)细胞是先天性免疫的一个组成部分,对B6小鼠抵抗鼠痘至关重要。然而,NK细胞介导的对OPV疾病的抵抗机制仍不明确。在这里,我们表明B6小鼠对鼠痘的抵抗力需要NK细胞的直接细胞溶解功能及其增强T细胞反应的能力。此外,我们表明激活受体NKG2D是NK细胞介导的对疾病和致死率的最佳抵抗力所必需的。总之,我们的结果对理解对致病性病毒感染的天然抵抗力具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/dd8fb7df7e13/ppat.0040030.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/525fede56f48/ppat.0040030.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/096a0dd33fa9/ppat.0040030.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/7775c02e044e/ppat.0040030.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/f94980f3818e/ppat.0040030.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/dd8fb7df7e13/ppat.0040030.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/525fede56f48/ppat.0040030.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/096a0dd33fa9/ppat.0040030.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/7775c02e044e/ppat.0040030.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/f94980f3818e/ppat.0040030.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeba/2323643/dd8fb7df7e13/ppat.0040030.g005.jpg

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