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MCPIP1 negatively regulate cellular antiviral innate immune responses through DUB and disruption of TRAF3-TBK1-IKKε

Xiaojuan Chen1, Qian Zhao1, Qing Xie1

  • 1Division of Infection and Immunity, Department of Biological Technology, Beijing Institute of Radiation Medicine, Beijing, 100850, China.

Biochemical and Biophysical Research Communications
|June 20, 2018
PubMed

Insights

Monocyte chemotactic protein-inducing protein 1 (MCPIP1) inhibits the innate immune response by blocking interferon-beta (IFNβ) expression. This protein disrupts the activation and nuclear translocation of IRF3, a key regulator of antiviral immunity.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Interferon-beta (IFNβ) is crucial for antiviral innate immunity.
  • Ubiquitination and de-ubiquitination (DUB) pathways regulate innate immune proteins.
  • Monocyte chemotactic protein-inducing protein 1 (MCPIP1) possesses DUB activity, but its role in IFNβ immunity is unclear.

Purpose of the Study:

  • To elucidate the mechanism by which MCPIP1 regulates IFNβ innate immune response.
  • To investigate MCPIP1's effect on key signaling molecules involved in IFNβ production.

Main Methods:

  • Investigated MCPIP1's effect on IFNβ expression induced by RIG-I, STING, TBK1, and IRF3.
  • Assessed MCPIP1's impact on IRF3 nuclear translocation.
  • Analyzed MCPIP1 interactions with IPS1, TRAF3, TBK1, and IKKε.
  • Examined MCPIP1's disruption of the TRAF3-TBK1-IKKε complex.

Main Results:

  • MCPIP1 negatively regulates IFNβ expression activated by RIG-I, STING, TBK1, and IRF3.
  • MCPIP1 inhibits the virus-induced nuclear translocation of IRF3, a critical step for type I IFN expression.
  • MCPIP1 interacts with IPS1, TRAF3, TBK1, and IKKε, disrupting the TRAF3-TBK1-IKKε complex.

Conclusions:

  • MCPIP1 acts as a host-encoded innate immune regulator.
  • MCPIP1 inhibits type I IFNβ expression by negatively regulating IRF3 activation.
  • A novel mechanism of MCPIP1-mediated inhibition of IFNβ innate immunity is described.
Keywords:
Antiviral innate immuneIRF3InterferonMCPIP1TRAF3-TBK1-IKKε complex

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