IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation

IL-23/IL-17 axis is an important regulator in various inflammatory diseases. However, the role of IL-23 in allergic airway inflammation is not well understood. In this study, we show that in an allergen-induced asthma model, mice with transgenic overexpression of IL-23R exhibited increased airway in...

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Detalles Bibliográficos
Autores principales: Peng, Juan, Yang, Xuexian O., Chang, Seon Hee, Yang, Jiong, Dong, Chen
Formato: Texto
Lenguaje:English
Publicado: 2009
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801763/
https://www.ncbi.nlm.nih.gov/pubmed/19935773
http://dx.doi.org/10.1038/cr.2009.128
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author Peng, Juan
Yang, Xuexian O.
Chang, Seon Hee
Yang, Jiong
Dong, Chen
author_facet Peng, Juan
Yang, Xuexian O.
Chang, Seon Hee
Yang, Jiong
Dong, Chen
author_sort Peng, Juan
collection PubMed
description IL-23/IL-17 axis is an important regulator in various inflammatory diseases. However, the role of IL-23 in allergic airway inflammation is not well understood. In this study, we show that in an allergen-induced asthma model, mice with transgenic overexpression of IL-23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production, whereas those deficient in IL-23 displayed reduced airway inflammation. In vitro, IL-23-IL-23R signaling promoted GATA-3 expression and enhanced Th2 cytokine expression. Conversely, in the absence of this signal, Th2 cell differentiation was partially inhibited. Therefore, IL-23 signaling may regulate allergic asthma through modulation of Th2 cell differentiation.
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spelling pubmed-28017632010-07-01 IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation Peng, Juan Yang, Xuexian O. Chang, Seon Hee Yang, Jiong Dong, Chen Cell Res Article IL-23/IL-17 axis is an important regulator in various inflammatory diseases. However, the role of IL-23 in allergic airway inflammation is not well understood. In this study, we show that in an allergen-induced asthma model, mice with transgenic overexpression of IL-23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production, whereas those deficient in IL-23 displayed reduced airway inflammation. In vitro, IL-23-IL-23R signaling promoted GATA-3 expression and enhanced Th2 cytokine expression. Conversely, in the absence of this signal, Th2 cell differentiation was partially inhibited. Therefore, IL-23 signaling may regulate allergic asthma through modulation of Th2 cell differentiation. 2009-11-24 2010-01 /pmc/articles/PMC2801763/ /pubmed/19935773 http://dx.doi.org/10.1038/cr.2009.128 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
Peng, Juan
Yang, Xuexian O.
Chang, Seon Hee
Yang, Jiong
Dong, Chen
IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title_full IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title_fullStr IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title_full_unstemmed IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title_short IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
title_sort il-23 signaling enhances th2 polarization and regulates allergic airway inflammation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801763/
https://www.ncbi.nlm.nih.gov/pubmed/19935773
http://dx.doi.org/10.1038/cr.2009.128
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AT yangjiong il23signalingenhancesth2polarizationandregulatesallergicairwayinflammation
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