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The transcription factor MafB antagonizes antiviral responses by blocking recruitment of coactivators to the

Hwijin Kim1, Brian Seed

  • 1Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts, USA.

Nature Immunology
|June 29, 2010
PubMed

Insights

The transcription factor MafB prevents self-amplification of antiviral responses by acting as a switch. Higher MafB levels in pancreatic cells may increase vulnerability to viral infections linked to type 1 diabetes.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Viral infections trigger type I interferons (IFN-alpha, IFN-beta) for self-amplifying immune responses.
  • These interferons recruit unexposed cells, amplifying the antiviral defense.

Purpose of the Study:

  • To investigate the role of the transcription factor MafB in regulating the auto-amplification of type I interferon responses.
  • To understand how MafB modulates the transcriptional activity at the IFNB1 promoter during viral infections.

Main Methods:

  • Analysis of MafB's transcriptional regulatory activity at the IFNB1 promoter.
  • Investigating MafB's interaction with IRF3 and coactivators upon interferon induction.
  • Utilizing mathematical modeling to simulate the dynamic response of the interferon system.

Main Results:

  • MafB functions as a weak positive regulator at the IFNB1 promoter under basal conditions.
  • Upon interferon elicitation, MafB acts as a transcriptional antagonist, inhibiting coactivator interaction with IRF3.
  • Mathematical modeling supports MafB's role in enabling rapid responses to IRF3 fluctuations.

Conclusions:

  • MafB acts as a metastable switch, preventing excessive auto-amplification of antiviral interferon responses.
  • Elevated MafB expression in pancreatic islet beta cells could enhance susceptibility to viral infections implicated in type 1 diabetes etiology.

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