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

被引:1141
作者
Sato, M
Suemori, H
Hata, N
Asagiri, M
Ogasawara, K
Nakao, K
Nakaya, T
Katsuki, M
Noguchi, S
Tanaka, N
Taniguchi, T
机构
[1] Univ Tokyo, Grad Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1130033, Japan
[2] Univ Tokyo, Fac Med, Bunkyo Ku, Tokyo 1130033, Japan
[3] Kanagawa Acad Sci & Technol, Bio Signal Pathway Project, Odawara, Kanagawa 2500862, Japan
[4] Meiji Milk Prod Co Ltd, Odawara, Kanagawa 2500862, Japan
[5] Univ Tokyo, Inst Med Sci, Dept DNA Biol & Embryo Engn, Minato Ku, Tokyo 1068639, Japan
关键词
D O I
10.1016/S1074-7613(00)00053-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 the two factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.
引用
收藏
页码:539 / 548
页数:10
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