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首页> 外文期刊>Journal of interferon and cytokine research: The official journal of the International Society for Interferon and Cytokine Research >IFN-beta-mediated inhibition of IL-8 expression requires the ISGF3 components Stat1, Stat2, and IRF-9.
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IFN-beta-mediated inhibition of IL-8 expression requires the ISGF3 components Stat1, Stat2, and IRF-9.

机译：IFN-β介导的IL-8表达抑制需要ISGF3组件Stat1，Stat2和IRF-9。

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摘要

Interleukin-8 (IL-8) is a key component of the innate immune response because of its ability to recruit inflammatory cells to sites of inflammation. Although the effects of IL-8 are largely beneficial, aberrant expression of IL-8 is known to contribute to a number of pathologic states. Interferon-beta (IFN-beta), an antiviral cytokine, is known to inhibit the expression of IL-8, although the exact mechanism by which this occurs has yet to be elucidated. In this study, we dissect the role of each member of the IFN-stimulated gene factor 3 (ISGF3) signaling complex in contributing to IFN-beta inhibition of IL-8 gene expression. To date, no IFN-stimulated response element (ISRE) (the DNA binding target for ISGF3) has been identified within the promoter region of the IL-8 gene. We conclude, through use of cell lines deficient for ISGF3 components, that all three members of this complex, Stat1, Stat2, and IFN regulatory factor-9 (IRF-9), are required for IFN-beta-mediated inhibition of IL-8 expression. In contrast to positive signaling by ISGF3 to activate gene expression, we find that the transactivation domains of Stat1 and Stat2 are not essential to IFN-beta inhibition of IL-8. Taken together, these data define the role of the ISGF3 members in IFN-beta inhibitory signaling.
机译：白介素8（IL-8）是先天免疫反应的关键组成部分，因为它具有将炎症细胞募集到炎症部位的能力。尽管IL-8的作用在很大程度上是有益的，但已知IL-8的异常表达会导致许多病理状态。已知干扰素-β（IFN-β）是一种抗病毒细胞因子，可抑制IL-8的表达，尽管其确切机制尚未阐明。在这项研究中，我们剖析了IFN刺激的基因因子3（ISGF3）信号复合物的每个成员在促成IFN-β抑制IL-8基因表达中的作用。迄今为止，尚未在IL-8基因的启动子区域内鉴定出IFN刺激的应答元件（ISRE）（ISGF3的DNA结合靶标）。我们得出结论，通过使用缺乏ISGF3成分的细胞系，该复合物的所有三个成员Stat1，Stat2和IFN调节因子9（IRF-9）都是IFN-β介导的IL-8抑制所必需的表达。与通过ISGF3激活基因表达的积极信号相反，我们发现Stat1和Stat2的反式激活域对于IFN-β抑制IL-8并不是必需的。综上所述，这些数据定义了ISGF3成员在IFN-β抑制信号传导中的作用。

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