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

Despite the paradigm that the innate immune system uses nucleic acid-specific receptors to detect viruses due to a lack of other conserved features, a number of viruses are recognized by TLR2 and TLR4. The relevance of this recognition for antiviral immunity remains largely unexplained. Here we repo...

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Detalles Bibliográficos
Autores principales: Barbalat, Roman, Lau, Laura, Locksley, Richard M., Barton, Gregory M.
Formato: Texto
Lenguaje:English
Publicado: 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821672/
https://www.ncbi.nlm.nih.gov/pubmed/19801985
http://dx.doi.org/10.1038/ni.1792
Descripción
Sumario:Despite the paradigm that the innate immune system uses nucleic acid-specific receptors to detect viruses due to a lack of other conserved features, a number of viruses are recognized by TLR2 and TLR4. The relevance of this recognition for antiviral immunity remains largely unexplained. Here we report that TLR2 activation by viruses leads to production of type I interferon (IFN). TLR2-dependent induction of type I IFN only occurs in response to viral ligands, indicating that TLR2 is capable of discriminating between pathogen classes. We demonstrate that this specialized response is mediated by Ly6C(high) inflammatory monocytes. Thus, the innate immune system can detect certain non-nucleic acid features of viruses and links this recognition to specific antiviral gene induction.