Toll-like receptor 2 on inflammatory monocytes induces type I interferon in response to viral but not bacterial ligands

Nat Immunol. 2009 Nov;10(11):1200-7. doi: 10.1038/ni.1792. Epub 2009 Oct 4.


Despite the paradigm that the innate immune system uses nucleic acid-specific receptors to detect viruses because of a lack of other conserved features, many viruses are recognized by Toll-like receptor 2 (TLR2) and TLR4. The relevance of this recognition for antiviral immunity remains largely unexplained. Here we report that TLR2 activation by viruses led to the production of type I interferon. TLR2-dependent induction of type I interferon occurred only in response to viral ligands, which indicates that TLR2 is able to discriminate between pathogen classes. We demonstrate that this specialized response was mediated by Ly6C(hi) inflammatory monocytes. Thus, the innate immune system can detect certain non-nucleic acid features of viruses and links this recognition to the induction of specific antiviral genes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD11 Antigens / immunology
  • Cell Line
  • Cricetinae
  • Flow Cytometry
  • Humans
  • Immunity, Innate
  • Interferon Type I / immunology*
  • Interferon Type I / metabolism
  • Ligands
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / immunology*
  • Monocytes / virology
  • Signal Transduction
  • Spleen / cytology
  • Spleen / immunology
  • Toll-Like Receptor 2 / immunology*
  • Toll-Like Receptor 2 / metabolism
  • Vaccinia / immunology*
  • Vaccinia virus / immunology


  • CD11 Antigens
  • Interferon Type I
  • Ligands
  • Tlr2 protein, mouse
  • Toll-Like Receptor 2