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

Authors: Peng, J  Yang, XO  Chang, SH  Yang, J  Dong, C 
Citation: Peng J, etal., Cell Res. 2010 Jan;20(1):62-71. Epub 2009 Nov 24.
Pubmed: (View Article at PubMed) PMID:19935773
DOI: Full-text: DOI:10.1038/cr.2009.128

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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CRRD Object Information
CRRD ID: 5037240
Created: 2011-03-03
Species: All species
Last Modified: 2011-03-03
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.