期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 213, 期 2, 页码 225-233出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20150712
关键词
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资金
- Medical Scientist Training Program [T32GM07739]
- National Institutes of Health [T32AI007621, AI068129, AI085034, AI100874, P30CA008748]
- Cancer Research Institute
- German Academic Exchange Service (DAAD) [57070483]
- Lucille Castori Center for Microbes, Inflammation, and Cancer
- Searle Scholars Program
Type I interferon (IFN) is crucial in host antiviral defense. Previous studies have described the pleiotropic role of type I IFNs on innate and adaptive immune cells during viral infection. Here, we demonstrate that natural killer (NK) cells from mice lacking the type I IFN-alpha receptor (Ifnar(-/-)) or STAT1 (which signals downstream of IFNAR) are defective in expansion and memory cell formation after mouse cytomegalovirus (MCMV) infection. Despite comparable proliferation, Ifnar(-/-) NK cells showed diminished protection against MCMV infection and exhibited more apoptosis compared with wild-type NK cells. Furthermore, we show that Ifnar(-/-) NK cells express increased levels of NK group 2 member D (NKG2D) ligands during viral infection and are susceptible to NK cell-mediated fratricide in a perforin- and NKG2D-dependent manner. Adoptive transfer of Ifnar(-/-) NK cells into NK cell-deficient mice reverses the defect in survival and expansion. Our study reveals a novel type I IFN-dependent mechanism by which NK cells evade mechanisms of cell death after viral infection.
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