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The complement C1qA enhances retinoic acid-inducible gene-I-mediated immune signalling

机译:补体C1qA增强视黄酸诱导的基因-I介导的免疫信号传导

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摘要

The cellular innate immune response is essential for recognizing and defending against viral infection. Retinoic acid-inducible gene-I (RIG-I) and virus-induced signaling adaptor (VISA) mediated immune signalling is critically involved in RNA-virus-induced innate immune responses. Here we demonstrate that the complement C1qA interacts with different RIG-I pathway components and enhances RIG-I-VISA-mediated signalling pathway as well as TBK1-mediated activation of interferon-β (IFN-β) promoter. Our data show that over-expression of C1qA up-regulates RIG-I-mediated activation of IFN-stimulated responsive element (ISRE) and nuclear factor-κB reporters and IFN-β transcription, but not IFN regulatory factor-3-mediated and inhibitor of κB kinase-mediated activation of ISRE and nuclear factor-κB promoter. In addition, C1qA can counteract the function of the C1q receptor gC1qR in RIG-I-mediated signalling. Our results reveal the important role of complement C1qA in the innate immune response.
机译:细胞先天免疫应答对于识别和防御病毒感染至关重要。维甲酸诱导的基因-I(RIG-I)和病毒诱导的信号衔接子(VISA)介导的免疫信号传导,与RNA病毒诱导的先天免疫反应密切相关。在这里,我们证明补体C1qA与不同的RIG-I途径组分相互作用并增强RIG-I-VISA介导的信号传导途径以及TBK1介导的干扰素-β(IFN-β)启动子的激活。我们的数据表明,C1qA的过表达上调了RIG-I介导的IFN刺激的响应元件(ISRE)和核因子-κB报道分子和IFN-β转录的激活,但不干扰IFN调节因子3介导的抑制剂κB激酶介导的ISRE活化和核因子-κB启动子的表达。另外,C1qA可以抵消RIG-I介导的信号传导中C1q受体gC1qR的功能。我们的结果揭示了补体C1qA在先天免疫反应中的重要作用。

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