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Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide
Regulatory CD4 T cells (Treg) control inflammatory reactions to commensal bacteria and opportunist pathogens. Activation of Treg functions during these processes might be mediated by host-derived proinflammatory molecules or directly by bacterial products. We tested the hypothesis that engagement of...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193858/ https://www.ncbi.nlm.nih.gov/pubmed/12591899 http://dx.doi.org/10.1084/jem.20021633 |
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author | Caramalho, Iris Lopes-Carvalho, Thiago Ostler, Dominique Zelenay, Santiago Haury, Matthias Demengeot, Jocelyne |
author_facet | Caramalho, Iris Lopes-Carvalho, Thiago Ostler, Dominique Zelenay, Santiago Haury, Matthias Demengeot, Jocelyne |
author_sort | Caramalho, Iris |
collection | PubMed |
description | Regulatory CD4 T cells (Treg) control inflammatory reactions to commensal bacteria and opportunist pathogens. Activation of Treg functions during these processes might be mediated by host-derived proinflammatory molecules or directly by bacterial products. We tested the hypothesis that engagement of germline-encoded receptors expressed by Treg participate in the triggering of their function. We report that the subset of CD4 cells known to exert regulatory functions in vivo (CD45RB(low) CD25(+)) selectively express Toll-like receptors (TLR)-4, -5, -7, and -8. Exposure of CD4(+) CD25(+) cells to the TLR-4 ligand lipopolysaccharide (LPS) induces up-regulation of several activation markers and enhances their survival/proliferation. This proliferative response does not require antigen-presenting cells and is augmented by T cell receptor triggering and interleukin 2 stimulation. Most importantly, LPS treatment increases CD4(+) CD25(+) cell suppressor efficiency by 10-fold and reveals suppressive activity in the CD4(+) CD45RB(low) CD25(−) subset that when tested ex-vivo, scores negative. Moreover, LPS-activated Treg efficiently control naive CD4 T cell–dependent wasting disease. These findings provide the first evidence that Treg respond directly to proinflammatory bacterial products, a mechanism that likely contributes to the control of inflammatory responses. |
format | Text |
id | pubmed-2193858 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21938582008-04-11 Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide Caramalho, Iris Lopes-Carvalho, Thiago Ostler, Dominique Zelenay, Santiago Haury, Matthias Demengeot, Jocelyne J Exp Med Article Regulatory CD4 T cells (Treg) control inflammatory reactions to commensal bacteria and opportunist pathogens. Activation of Treg functions during these processes might be mediated by host-derived proinflammatory molecules or directly by bacterial products. We tested the hypothesis that engagement of germline-encoded receptors expressed by Treg participate in the triggering of their function. We report that the subset of CD4 cells known to exert regulatory functions in vivo (CD45RB(low) CD25(+)) selectively express Toll-like receptors (TLR)-4, -5, -7, and -8. Exposure of CD4(+) CD25(+) cells to the TLR-4 ligand lipopolysaccharide (LPS) induces up-regulation of several activation markers and enhances their survival/proliferation. This proliferative response does not require antigen-presenting cells and is augmented by T cell receptor triggering and interleukin 2 stimulation. Most importantly, LPS treatment increases CD4(+) CD25(+) cell suppressor efficiency by 10-fold and reveals suppressive activity in the CD4(+) CD45RB(low) CD25(−) subset that when tested ex-vivo, scores negative. Moreover, LPS-activated Treg efficiently control naive CD4 T cell–dependent wasting disease. These findings provide the first evidence that Treg respond directly to proinflammatory bacterial products, a mechanism that likely contributes to the control of inflammatory responses. The Rockefeller University Press 2003-02-17 /pmc/articles/PMC2193858/ /pubmed/12591899 http://dx.doi.org/10.1084/jem.20021633 Text en Copyright © 2003, 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 | Article Caramalho, Iris Lopes-Carvalho, Thiago Ostler, Dominique Zelenay, Santiago Haury, Matthias Demengeot, Jocelyne Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title | Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title_full | Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title_fullStr | Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title_full_unstemmed | Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title_short | Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide |
title_sort | regulatory t cells selectively express toll-like receptors and are activated by lipopolysaccharide |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193858/ https://www.ncbi.nlm.nih.gov/pubmed/12591899 http://dx.doi.org/10.1084/jem.20021633 |
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