MICE DEVOID OF INTERFERON REGULATORY FACTOR-1 (IRF-1) SHOW NORMAL EXPRESSION OF TYPE-I INTERFERON GENES

被引：169

作者：

REIS, LFL ^{[1
]}

RUFFNER, H ^{[1
]}

STARK, G ^{[1
]}

AGUET, M ^{[1
]}

WEISSMANN, C ^{[1
]}

机构：

[1] UNIV ZURICH, INST MOLEK BIOL 1, CH-8093 ZURICH, SWITZERLAND

来源：

EMBO JOURNAL | 1994年 / 13卷 / 20期

关键词：

INO SYNTHASE INDUCTION; INTERFERON GENE INDUCTION; INTERFERON-INDUCIBLE GENES; IRF-1; KNOCKOUT;

D O I：

10.1002/j.1460-2075.1994.tb06805.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：4798 / 4806

页数：9

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