期刊
JOURNAL OF IMMUNOLOGY
卷 189, 期 2, 页码 516-520出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1200064
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资金
- National Institutes of Health
- Crohn's and Colitis Foundation of America
- Cancer Research Institute
- Claudia Adams Barr Award
- European Molecular Biology Organization Long-Term fellowship
- Crohn's Colitis Foundation of America fellowship
MHC class I and class II are crucial for the adaptive immune system. Although regulation of MHC class II expression by CIITA has long been recognized, the mechanism of MHC class I transactivation has been largely unknown until the recent discovery of NLRC5/class I transactivator. In this study, we show using Nlrc5-deficient mice that NLRC5 is required for both constitutive and inducible MHC class I expression. Loss of Nlrc5 resulted in severe reduction in the expression of MHC class I and related genes such as beta(2)-microglobulin, Tap1, or Lmp2, but did not affect MHC class II levels. IFN-gamma stimulation could not overcome the impaired MHC class I expression in Nlrc5-deficient cells. Upon infection with Listeria monocyogenes, Nlrc5-deficient mice displayed impaired CD8(+) T cell activation, accompanied with increased bacterial loads. These findings illustrate critical roles of NLRC5/class I transactivator in MHC class I gene regulation and host defense by CD8(+) T cell responses. The Journal of Immunology, 2012, 189: 516-520.
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