Format

Send to

Choose Destination
Cell Res. 2010 Jan;20(1):62-71. doi: 10.1038/cr.2009.128. Epub 2009 Nov 24.

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

Author information

1
Department of Immunology, MD Anderson Cancer Center, Houston, TX 77030, USA.

Abstract

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.

PMID:
19935773
PMCID:
PMC2801763
DOI:
10.1038/cr.2009.128
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center