期刊
PLOS PATHOGENS
卷 4, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1000106
关键词
-
资金
- National Institutes of Health [AI46709, AI058181]
- NCCR [1S10RR021051]
- undergraduate Royce fellowship
- U. S. Department of Education Pre-Doctoral Training [P200A000117]
Immunity to the murine cytomegalovirus (MCMV) is critically dependent on the innate response for initial containment of viral replication, resolution of active infection, and proper induction of the adaptive phase of the anti-viral response. In contrast to NK cells, the V alpha 14 invariant natural killer T cell response to MCMV has not been examined. We found that V alpha 14i NK T cells become activated and produce significant levels of IFN-gamma, but do not proliferate or produce IL-4 following MCMV infection. In vivo treatment with an anti-CD1d mAb and adoptive transfer of V alpha 14i NK T cells into MCMV-infected CD1d(-/)-mice demonstrate that CD1d is dispensable for Va14i NK T cell activation. In contrast, both IFN-alpha/beta and IL-12 are required for optimal activation. V alpha 14i NK T cell-derived IFN-gamma is partially dependent on IFN-alpha/beta but highly dependent on IL-12. V alpha 14i NK T cells contribute to the immune response to MCMV and amplify NK cell-derived IFN-c. Importantly, mortality is increased in CD1d 2/2 mice in response to high dose MCMV infection when compared to heterozygote littermate controls. Collectively, these findings illustrate the plasticity of V alpha 14i NK T cells that act as effector T cells during bacterial infection, but have NK cell-like behavior during the innate immune response to MCMV infection.
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