Sato M, Suemori H, Hata N, Asagiri M, Ogasawara K, Nakao K, Nakaya T, Katsuki M, Noguchi S, Tanaka N, Taniguchi T
Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Japan.
Immunity. 2000 Oct;13(4):539-48. doi: 10.1016/s1074-7613(00)00053-4.
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.
病毒感染细胞中干扰素（IFN）-α/β基因转录的诱导是先天免疫的核心事件。缺乏转录因子IRF-3的小鼠更容易受到病毒感染。在胚胎成纤维细胞中，病毒诱导的IFN-α/β基因表达水平降低，且IFN-α mRNA亚群的谱发生改变。此外，IRF-7表达额外存在缺陷的细胞在受到任何测试病毒类型感染时完全无法诱导这些基因。在这些细胞中，通过共表达IRF-3和IRF-7可实现IFN-α/β mRNA诱导的正常谱。这些结果证明了这两种因子的重要且不同的作用，它们共同确保了IFN-α/β基因在抗病毒反应中的转录效率和多样性。
