Journal
PLOS PATHOGENS
Volume 4, Issue 2, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.0040030
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Funding
- NCI NIH HHS [CA006927, P30 CA006927] Funding Source: Medline
- NIAID NIH HHS [AI065544, R01 AI065544, R01 AI048849, AI066897, AI048849, R37 AI066897] Funding Source: Medline
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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.
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