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The complement C1qA enhances retinoic acid-inducible gene-I-mediated immune signalling
Yetao Wang1, Xiaomei Tong, Junjie Zhang
1Centre for Molecular Immunology, CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Abstract:
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.
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