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Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses

Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with CD4(+) Th cells determining both disease severity and resistance to infection. Th2 cell responses promote immunopathology, while Th1 cells c...

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Autores principales: Odeh, Adam N., Simecka, Jerry W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866680/
https://www.ncbi.nlm.nih.gov/pubmed/27175511
http://dx.doi.org/10.1371/journal.pone.0155648
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author Odeh, Adam N.
Simecka, Jerry W.
author_facet Odeh, Adam N.
Simecka, Jerry W.
author_sort Odeh, Adam N.
collection PubMed
description Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with CD4(+) Th cells determining both disease severity and resistance to infection. Th2 cell responses promote immunopathology, while Th1 cells confer resistance to infection. However, regulatory CD4(+) T cells may also have a role in the pathogenesis of mycoplasma respiratory diseases. We hypothesized Treg cells control the severity of the inflammatory lesions and may also promote persistence of infection. To examine this, BALB/c mice were depleted of CD25(+) cells, and had increased disease severity due to Mycoplasma pulmonis infection. Increases in mycoplasma antibody responses and lymphocyte infiltration into lungs also occurred after CD25(+) cell depletion. CD4(+)CD25(+) regulatory T cells promoted IFN-γ and IL-17 mycoplasma-specific CD4(+) T cell responses in vitro and in vivo, while dampening IL-13(+) Th responses. Neither IL-10 nor TGF-ß expression was detected in CD4(+)CD25(+) T cells from lymph nodes. Thus, a regulatory T cell population plays an important role in controlling damaging immune responses in mycoplasma respiratory disease but does not contribute to persistence of infection. It appears that a regulatory T cell population preferentially dampens Th2 cell-mediated inflammatory responses to mycoplasma through a mechanism independent of IL-10 or TGF-ß characteristic of “classic” Treg cells.
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spelling pubmed-48666802016-05-18 Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses Odeh, Adam N. Simecka, Jerry W. PLoS One Research Article Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with CD4(+) Th cells determining both disease severity and resistance to infection. Th2 cell responses promote immunopathology, while Th1 cells confer resistance to infection. However, regulatory CD4(+) T cells may also have a role in the pathogenesis of mycoplasma respiratory diseases. We hypothesized Treg cells control the severity of the inflammatory lesions and may also promote persistence of infection. To examine this, BALB/c mice were depleted of CD25(+) cells, and had increased disease severity due to Mycoplasma pulmonis infection. Increases in mycoplasma antibody responses and lymphocyte infiltration into lungs also occurred after CD25(+) cell depletion. CD4(+)CD25(+) regulatory T cells promoted IFN-γ and IL-17 mycoplasma-specific CD4(+) T cell responses in vitro and in vivo, while dampening IL-13(+) Th responses. Neither IL-10 nor TGF-ß expression was detected in CD4(+)CD25(+) T cells from lymph nodes. Thus, a regulatory T cell population plays an important role in controlling damaging immune responses in mycoplasma respiratory disease but does not contribute to persistence of infection. It appears that a regulatory T cell population preferentially dampens Th2 cell-mediated inflammatory responses to mycoplasma through a mechanism independent of IL-10 or TGF-ß characteristic of “classic” Treg cells. Public Library of Science 2016-05-13 /pmc/articles/PMC4866680/ /pubmed/27175511 http://dx.doi.org/10.1371/journal.pone.0155648 Text en © 2016 Odeh, Simecka http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Odeh, Adam N.
Simecka, Jerry W.
Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title_full Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title_fullStr Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title_full_unstemmed Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title_short Regulatory CD4(+)CD25(+) T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
title_sort regulatory cd4(+)cd25(+) t cells dampen inflammatory disease in murine mycoplasma pneumonia and promote il-17 and ifn-γ responses
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866680/
https://www.ncbi.nlm.nih.gov/pubmed/27175511
http://dx.doi.org/10.1371/journal.pone.0155648
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