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Mice devoid of interferon regulatory factor 1 (IRF-1) show normal expression of type I interferon genes.
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.
Animals, Cell Line, DNA-Binding Proteins/physiology, Female, Gene Expression Regulation/physiology, Interferon Regulatory Factor-1, Interferon Type I/genetics, Male, Mice, Mice, Inbred C57BL, Mice, Inbred ICR, Molecular Sequence Data, Phosphoproteins/physiology, Transcription Factors/physiology
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