PLoS Pathogens | |
A Role for NKG2D in NK Cell–Mediated Resistance to Poxvirus Disease | |
Luis J Sigal1  Lewis L Lanier2  Min Fang3  | |
[1] Cancer Research Institute, University of California San Francisco, San Francisco, California, United States of America;Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California, United States of America;Program of Viral Pathogenesis, Division of Basic Sciences, Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America | |
关键词: NK cells; T cells; Spleen; Antimicrobial resistance; Cytotoxic T cells; Cell staining; T cell receptors; Cytotoxicity; | |
DOI : 10.1371/journal.ppat.0040030 | |
学科分类:生物科学(综合) | |
来源: Public Library of Science | |
【 摘 要 】
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.
【 授权许可】
CC BY
【 预 览 】
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RO201902011733301ZK.pdf | 500KB | download |