MICE DEVOID OF INTERFERON REGULATORY FACTOR-1 (IRF-1) SHOW NORMAL EXPRESSION OF TYPE-I INTERFERON GENES
MICE DEVOID OF INTERFERON REGULATORY FACTOR-1 (IRF-1) SHOW NORMAL EXPRESSION OF TYPE-I INTERFERON GENES
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DOI：
10.1002/j.1460-2075.1994.tb06805.x
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发表时间：
1994-10-17
期刊：
影响因子：
11.4
通讯作者：
WEISSMANN, C
中科院分区：
文献类型：
--
作者：
REIS, LFL;RUFFNER, H;WEISSMANN, C
转录因子干扰素调节因子1 （IRF-1）与干扰素(IFN)- β启动子紧密结合，并与I型IFN的诱导有关。我们通过靶向基因破坏产生了缺乏功能性IRF-1的小鼠。据其他报道，irf -1缺陷小鼠表现出离散表型：CD4/CD8比值升高，ifn - γ诱导的巨噬细胞iNO合成酶mRNA水平强烈降低。然而，通过血清IFN滴度和脾脏、肝脏和肺部的IFN mRNA水平可以证明，病毒或双链RNA对体内I型IFN的诱导并未受损。I型ifn诱导基因的反应也没有损伤。因此，IRF-1在体内对这些过程并不是必需的。
The transcription factor interferon regulatory factor 1 (IRF-1) binds tightly to the interferon (IFN)-beta promoter and has been implicated in the induction of type I IFNs. We generated mice devoid of functional IRF-1 by targeted gene disruption. As reported by others, IRF-1-deficient mice showed a discrete phenotype: the CD4/CD8 ratio was increased and IFN-gamma-induced levels of macrophage iNO synthase mRNA were strongly diminished. However, type I IFN induction in vivo by virus or double-stranded RNA was unimpaired, as evidenced by serum IFN titers and IFN mRNA levels in spleen, liver and lung. There was also no impairment in the response of type I IFN-inducible genes. Therefore, IRF-1 is not essential for these processes irt vivo.