Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction.
Journal:
Immunity 2000 OctAuthors:
Sato M, Suemori H, Hata N, Asagiri M, Ogasawara K, Nakao K, Nakaya T, Katsuki M, Noguchi S, Tanaka N, Taniguchi T
Abstract
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 vi
...[more]rus 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.[less]
Mesh Headings:
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