| First Author | Biswas A | Year | 2012 |
| Journal | J Immunol | Volume | 189 |
| Issue | 2 | Pages | 516-20 |
| PubMed ID | 22711889 | Mgi Jnum | J:189799 |
| Mgi Id | MGI:5447005 | Doi | 10.4049/jimmunol.1200064 |
| Citation | Biswas A, et al. (2012) Cutting edge: impaired MHC class I expression in mice deficient for Nlrc5/class I transactivator. J Immunol 189(2):516-20 |
| abstractText | 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. |
