Interferon induction and function at the mucosal surface

Immunol Rev. 2013 Sep;255(1):25-39. doi: 10.1111/imr.12101.


Interferons (IFNs) are produced in response to virus infection and induce an antiviral state in virtually all cell types. In addition to upregulating the transcription of genes that inhibit virus replication, type I (or -α/β) IFNs also act to orchestrate the adaptive immune response to virus infection. Recently a new family of antiviral cytokines, the type III (or -λ) IFNs, has been identified that activate the same antiviral pathways via a distinct receptor. Although the identical transcription factor, IFN-stimulated gene factor 3 is activated by either IFN-α/β or IFN-λ signaling, differences in the induction and action of these two cytokine families are beginning to be appreciated. In this article, we review this emerging body of literature on the differing roles these cytokines play in host defense of the mucosal surface. Although many viruses enter the body through the respiratory and gastrointestinal tracts, we have focused the discussion on influenza A virus, respiratory syncytial virus, and rotavirus, three ubiquitous human pathogens that target the epithelial lining and are associated with a major disease burden.

Keywords: IFN induction; Stat signaling; influenza A virus; interferon; respiratory syncytial virus; rotavirus.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation
  • Humans
  • Interferons / immunology*
  • Interferons / metabolism*
  • Janus Kinases / metabolism
  • Ligands
  • Mucous Membrane / immunology*
  • Mucous Membrane / metabolism*
  • Mucous Membrane / virology
  • Phosphorylation
  • Protein Biosynthesis
  • STAT Transcription Factors / metabolism
  • Signal Transduction
  • Toll-Like Receptors / metabolism
  • Virus Diseases / genetics
  • Virus Diseases / immunology
  • Virus Diseases / metabolism
  • Viruses / immunology


  • Ligands
  • STAT Transcription Factors
  • Toll-Like Receptors
  • Interferons
  • Janus Kinases