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Journals Nature Volume 452 Issue 7185

Transcriptional activation of cytokines, such as type-I interferons (interferon (IFN)-ॅ and IFN-ॆ), constitutes the first line of antiviral defence. Here we show that translational control is critical for induction of type-I IFN production. In mouse embryonic fibroblasts lacking the translational repressors 4E-BP1 and 4E-BP2, the threshold for eliciting type-I IFN production is lowered. Consequently, replication of encephalomyocarditis virus, vesicular stomatitis virus, influenza virus and Sindbis virus is markedly suppressed. Furthermore, mice with both 4E- and 4E-BP2 genes (also known as Eif4ebp1 and Eif4ebp2 , respectively) knocked out are resistant to vesicular stomatitis virus infection, and this correlates with an enhanced type-I IFN production in plasmacytoid dendritic cells and the expression of IFN-regulated genes in the lungs. The enhanced type-I IFN response in 4E-BP1 -/- 4E-BP2 -/- double knockout mouse embryonic fibroblasts is caused by upregulation of interferon regulatory factor 7 ( Irf7 ) messenger RNA translation. These findings highlight the role of 4E-BPs as negative regulators of type-I IFN production, via translational repression of Irf7 mRNA.

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Translational control of the innate immune response through IRF-7

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  • Publisher Nature Publishing Group
  • Copyright Copyright © 2008 Nature Publishing Group
  • ISSN 0028-0836
  • eISSN 1476-4687
  • D.O.I. 10.1038/nature06730
  • Publisher site Get PDF  

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