期刊
IMMUNITY
卷 34, 期 4, 页码 579-589出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.02.015
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资金
- NIAID [R01AI048849, R21AI077021, R01AI065544]
- NIH [AI066897]
- NCI [CA006927]
- Cancer Research Institute
It is well established that natural killer (NK) cells confer resistance to many viral diseases, but in only a few instances the molecular mechanisms whereby NK cells recognize virus-infected cells are known. Here we show that CD94, a molecule preferentially expressed by NK cells, is essential for the resistance of C57BL/6 mice to mousepox, a disease caused by the Orthopoxvirus ectromelia virus. Ectromelia virus-infected cells expressing the major histocompatibility complex (MHC) class lb molecule Qa-1(b) are specifically recognized by the activating receptor formed by CD94 and NKG2E. Because CD94-NKG2 receptors and their ligands are highly conserved in rodents and humans, a similar mechanism may exist during human infections with the smallpox and monkeypox viruses, which are highly homologous to ectromelia virus.
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