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Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo

Dendritic cell (DC) activation is a prerequisite for T cell priming. During infection, activation can ensue from signaling via pattern-recognition receptors after contact with pathogens or infected cells. Alternatively, it has been proposed that DCs can be activated indirectly by signals produced by...

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Autores principales: Nolte, Martijn A., LeibundGut-Landmann, Salomé, Joffre, Olivier, Sousa, Caetano Reis e
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118612/
https://www.ncbi.nlm.nih.gov/pubmed/17548522
http://dx.doi.org/10.1084/jem.20070325
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author Nolte, Martijn A.
LeibundGut-Landmann, Salomé
Joffre, Olivier
Sousa, Caetano Reis e
author_facet Nolte, Martijn A.
LeibundGut-Landmann, Salomé
Joffre, Olivier
Sousa, Caetano Reis e
author_sort Nolte, Martijn A.
collection PubMed
description Dendritic cell (DC) activation is a prerequisite for T cell priming. During infection, activation can ensue from signaling via pattern-recognition receptors after contact with pathogens or infected cells. Alternatively, it has been proposed that DCs can be activated indirectly by signals produced by infected tissues. To address the contribution of tissue-derived signals, we measured DC activation in a model in which radioresistant cells can or cannot respond to lipopolysaccharide (LPS). We report that recognition of LPS by the radioresistant compartment is sufficient to induce local and systemic inflammation characterized by high circulating levels of tumor necrosis factor (TNF) α, interleukin (IL) 1β, IL-6, and CC chemokine ligand 2. However, this is not sufficient to activate DCs, whether measured by migration, gene expression, phenotypic, or functional criteria, or to render DC refractory to subsequent stimulation with CpG-containing DNA. Similarly, acute or chronic exposure to proinflammatory cytokines such as TNF-α ± interferon α/β has marginal effects on DC phenotype in vivo when compared with LPS. In addition, DC activation and migration induced by LPS is unimpaired when radioresistant cells cannot respond to the stimulus. Thus, inflammatory mediators originating from nonhematopoietic tissues and from radioresistant hematopoietic cells are neither sufficient nor required for DC activation in vivo.
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spelling pubmed-21186122007-12-13 Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo Nolte, Martijn A. LeibundGut-Landmann, Salomé Joffre, Olivier Sousa, Caetano Reis e J Exp Med Articles Dendritic cell (DC) activation is a prerequisite for T cell priming. During infection, activation can ensue from signaling via pattern-recognition receptors after contact with pathogens or infected cells. Alternatively, it has been proposed that DCs can be activated indirectly by signals produced by infected tissues. To address the contribution of tissue-derived signals, we measured DC activation in a model in which radioresistant cells can or cannot respond to lipopolysaccharide (LPS). We report that recognition of LPS by the radioresistant compartment is sufficient to induce local and systemic inflammation characterized by high circulating levels of tumor necrosis factor (TNF) α, interleukin (IL) 1β, IL-6, and CC chemokine ligand 2. However, this is not sufficient to activate DCs, whether measured by migration, gene expression, phenotypic, or functional criteria, or to render DC refractory to subsequent stimulation with CpG-containing DNA. Similarly, acute or chronic exposure to proinflammatory cytokines such as TNF-α ± interferon α/β has marginal effects on DC phenotype in vivo when compared with LPS. In addition, DC activation and migration induced by LPS is unimpaired when radioresistant cells cannot respond to the stimulus. Thus, inflammatory mediators originating from nonhematopoietic tissues and from radioresistant hematopoietic cells are neither sufficient nor required for DC activation in vivo. The Rockefeller University Press 2007-06-11 /pmc/articles/PMC2118612/ /pubmed/17548522 http://dx.doi.org/10.1084/jem.20070325 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Nolte, Martijn A.
LeibundGut-Landmann, Salomé
Joffre, Olivier
Sousa, Caetano Reis e
Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title_full Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title_fullStr Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title_full_unstemmed Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title_short Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo
title_sort dendritic cell quiescence during systemic inflammation driven by lps stimulation of radioresistant cells in vivo
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118612/
https://www.ncbi.nlm.nih.gov/pubmed/17548522
http://dx.doi.org/10.1084/jem.20070325
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