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

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-beta (IFN-beta) promoter. Our data show that over-expression of C1qA up-regulates RIG-I-mediated activation of IFN-stimulated responsive element (ISRE) and nuclear factor-?B reporters and IFN-beta transcription, but not IFN regulatory factor-3-mediated and inhibitor of ?B kinase-mediated activation of ISRE and nuclear factor-?B 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.