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

Immunology. 2012 May;136(1):78-85. doi: 10.1111/j.1365-2567.2012.03561.x.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Complement C1q / immunology*
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / genetics
  • DEAD-box RNA Helicases / immunology*
  • DEAD-box RNA Helicases / metabolism
  • Dogs
  • Humans
  • Immunity, Innate
  • Interferon-beta / immunology
  • Interferon-beta / metabolism
  • NF-kappa B / immunology
  • NF-kappa B / metabolism
  • Receptors, Immunologic
  • Signal Transduction*

Substances

  • NF-kappa B
  • Receptors, Immunologic
  • Interferon-beta
  • Complement C1q
  • RIGI protein, human
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases