Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction.
Induction of the interferon (IFN)-alpha/beta gene transcription in virus-infected cells is an event central to innate immunity. Mice lacking the transcription factor IRF-3 are more vulnerable to virus infection. In embryonic fibroblasts, virus-induced IFN-alpha/beta gene expression levels are reduced and the spectrum of the IFN-alpha mRNA subspecies altered. Furthermore, cells additionally defective in IRF-7 expression totally fail to induce these genes in response to infections by any of the virus types tested. In these cells, a normal profile of IFN-alpha/beta mRNA induction can be achieved by coexpressing both IRF-3 and IRF-7. These results demonstrate the essential and distinct roles of thetwo factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.
Pubmed ID: 11070172 RIS Download
Animals | DNA-Binding Proteins | Down-Regulation | Embryo, Mammalian | Female | Fibroblasts | Gene Expression Regulation | Gene Targeting | Interferon Regulatory Factor-3 | Interferon Regulatory Factor-7 | Interferon Type I | Interferon-beta | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Mice, Transgenic | Newcastle disease virus | Promoter Regions, Genetic | RNA, Messenger | Retroviridae | Signal Transduction | Transcription Factors | Transcriptional Activation