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Distinct and Essential Roles of Transcription Factors IRF-3 and IRF-7 in Response to Viruses forIFN-α/βGene Induction

Authors
Publisher
Elsevier Inc.
Publication Date
Volume
13
Issue
4
Identifiers
DOI: 10.1016/s1074-7613(00)00053-4

Abstract

Abstract Induction of the interferon (IFN)-α/β 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-α/β gene expression levels are reduced and the spectrum of the IFN-α 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-α/β mRNA induction can be achieved by coexpressing both IRF-3 and IRF-7. These results demonstrate the essential and distinct roles of the two factors, which together ensure the transcriptional efficiency and diversity of IFN-α/β genes for the antiviral response.

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