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缺乏干扰素调节因子1（IRF-1）的小鼠表现出I型干扰素基因的正常表达。

Mice devoid of interferon regulatory factor 1 (IRF-1) show normal expression of type I interferon genes.

作者信息

Reis L F, Ruffner H, Stark G, Aguet M, Weissmann C

机构信息

Institut für Molekularbiologie I, Universität Zürich, Switzerland.

出版信息

EMBO J. 1994 Oct 17;13(20):4798-806. doi: 10.1002/j.1460-2075.1994.tb06805.x.

DOI:10.1002/j.1460-2075.1994.tb06805.x
PMID:7957048
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC395418/
Abstract

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 in vivo.

摘要

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型干扰素的诱导有关。我们通过靶向基因破坏产生了缺乏功能性IRF-1的小鼠。正如其他人所报道的，IRF-1缺陷小鼠表现出一种离散的表型：CD4/CD8比率增加，IFN-γ诱导的巨噬细胞诱导型一氧化氮合酶mRNA水平显著降低。然而，病毒或双链RNA在体内诱导I型干扰素的能力并未受损，血清干扰素滴度以及脾脏、肝脏和肺中的干扰素mRNA水平证明了这一点。I型干扰素诱导基因的反应也没有受损。因此，IRF-1在体内对于这些过程并非必不可少。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/dcd03f2c4410/emboj00068-0101-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/6ae59c50f277/emboj00068-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/d3117385e5c6/emboj00068-0096-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/c950ab6783f7/emboj00068-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/88c67e3f076a/emboj00068-0097-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/95dd4c729839/emboj00068-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/1d49d5b9ab02/emboj00068-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/8faff2e461b5/emboj00068-0100-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/dcd03f2c4410/emboj00068-0101-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/6ae59c50f277/emboj00068-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/d3117385e5c6/emboj00068-0096-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/c950ab6783f7/emboj00068-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/88c67e3f076a/emboj00068-0097-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/95dd4c729839/emboj00068-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/1d49d5b9ab02/emboj00068-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/8faff2e461b5/emboj00068-0100-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6765/395418/dcd03f2c4410/emboj00068-0101-a.jpg

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