期刊
JOURNAL OF INFECTIOUS DISEASES
卷 189, 期 4, 页码 658-668出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/381501
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Type 1 interferon (IFN) receptor gene knockout (IFNAR(-/-)) mouse embryo fibroblasts (MEFs) are more susceptible to and productive of West Nile virus (WNV) and produce less type 1 IFN than WNV-infected wildtype (wt) MEFs. WNV infection of eIFNAR(-/-) MEFs induced activation of a p65/p50 heterodimer of nuclear factor (NF)-kappaB and up-regulation of cell-surface expression of major histocompatibility complex class I (MHC-I) molecules. WNV infection of wt MEFs resulted in a greater up-regulation of MHC-I than did infection of IFNAR(-/-) MEFs because of the action of endogenous type 1 IFN production. IFN-beta-treatment of wt MEFs did not activate NF-kappaB but did up-regulate cell-surface MHC-I expression. The WNV-induced NF-kappaB activation was partially abrogated by the serine protease inhibitor N-benzoyl-L-tosyl-L-phenylalanine, which also abrogated the up-regulation of MHC-I. Thus, we demonstrate 2 pathways for WNV-induced up-regulation of MHCI, a WNV-induced NF-kappaB-dependent, IFN-independent pathway and an NF-kappaB-independent, IFN-dependent pathway.
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