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      Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction.

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          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 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.

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          Author and article information

          Journal
          Immunity
          Immunity
          Elsevier BV
          1074-7613
          1074-7613
          Oct 2000
          : 13
          : 4
          Affiliations
          [1 ] Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Japan.
          Article
          S1074-7613(00)00053-4
          10.1016/s1074-7613(00)00053-4
          11070172
          83e7b533-2c02-44ce-a20d-668d3aaf9421
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