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IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus

Immune responses to vaccines require direct recognition of pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) on dendritic cells (DCs). Unlike vaccines, infection by a live pathogen often impairs DC function and inflicts additional damage to the host. Here, w...

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Detalles Bibliográficos
Autores principales: Pang, Iris K., Ichinohe, Takeshi, Iwasaki, Akiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577947/
https://www.ncbi.nlm.nih.gov/pubmed/23314004
http://dx.doi.org/10.1038/ni.2514
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author Pang, Iris K.
Ichinohe, Takeshi
Iwasaki, Akiko
author_facet Pang, Iris K.
Ichinohe, Takeshi
Iwasaki, Akiko
author_sort Pang, Iris K.
collection PubMed
description Immune responses to vaccines require direct recognition of pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) on dendritic cells (DCs). Unlike vaccines, infection by a live pathogen often impairs DC function and inflicts additional damage to the host. Here, we found that following live influenza A infection, signaling through the interleukin-1 receptor (IL-1R), but not the PRRs, TLR7 and RIG-I, is required for productive CD8(+) T cell priming. DCs activated by IL-1 in trans were both required and sufficient for the generation of virus-specific CD8(+) T cell immunity. Our data reveal a critical role of a bystander cytokine in CD8(+) T cell priming during a live viral infection.
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spelling pubmed-35779472013-09-01 IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus Pang, Iris K. Ichinohe, Takeshi Iwasaki, Akiko Nat Immunol Article Immune responses to vaccines require direct recognition of pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) on dendritic cells (DCs). Unlike vaccines, infection by a live pathogen often impairs DC function and inflicts additional damage to the host. Here, we found that following live influenza A infection, signaling through the interleukin-1 receptor (IL-1R), but not the PRRs, TLR7 and RIG-I, is required for productive CD8(+) T cell priming. DCs activated by IL-1 in trans were both required and sufficient for the generation of virus-specific CD8(+) T cell immunity. Our data reveal a critical role of a bystander cytokine in CD8(+) T cell priming during a live viral infection. 2013-01-13 2013-03 /pmc/articles/PMC3577947/ /pubmed/23314004 http://dx.doi.org/10.1038/ni.2514 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Pang, Iris K.
Ichinohe, Takeshi
Iwasaki, Akiko
IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title_full IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title_fullStr IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title_full_unstemmed IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title_short IL-1R signaling in dendritic cells replaces pattern recognition receptors to promote CD8(+) T cell responses to influenza A virus
title_sort il-1r signaling in dendritic cells replaces pattern recognition receptors to promote cd8(+) t cell responses to influenza a virus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577947/
https://www.ncbi.nlm.nih.gov/pubmed/23314004
http://dx.doi.org/10.1038/ni.2514
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