期刊
JOURNAL OF VIROLOGY
卷 86, 期 16, 页码 8713-8719出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00682-12
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资金
- Excellence Initiative of the German Federal Government (Spemann Graduate School) [GSC-4]
- Excellence Initiative of the German State Government (Spemann Graduate School) [GSC-4]
- Centre for Biological Signaling Studies (Bioss) by the Excellence Initiative of the German Federal Government [EXC 294]
- Centre for Biological Signaling Studies (Bioss) by the Excellence Initiative of the State Federal Government [EXC 294]
- Deutsche Forschungsgemeinschaft [BO-1933, GRK1104]
- [5RO1AI04494-03]
The T cell granule exocytosis pathway is essential to control hepatotropic lymphocytic choriomeningitis virus strain WE (LCMV-WE) but also contributes to the observed pathology in mice. Although effective antiviral T cell immunity and development of viral hepatitis are strictly dependent on perforin and granzymes, the molecular basis underlying induction of functionally competent virus-immune T cells, including participation of the innate immune system, is far from being resolved. We demonstrate here that LCMV-immune T cells of interleukin-1 receptor (IL-1R)-deficient mice readily express transcripts for perforin and granzymes but only translate perforin, resulting in the lack of proapoptotic potential in vitro. LCMV is not cleared in IL-1R-deficient mice, and yet the infected mice develop neither splenomegaly nor hepatitis. These results demonstrate that IL-1R signaling is central to the induction of proapoptotic CD8 T cell immunity, including viral clearance and associated tissue injuries in LCMV infection.
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