| First Author | Peng J | Year | 2010 |
| Journal | Cell Res | Volume | 20 |
| Issue | 1 | Pages | 62-71 |
| PubMed ID | 19935773 | Mgi Jnum | J:221933 |
| Mgi Id | MGI:5642094 | Doi | 10.1038/cr.2009.128 |
| Citation | Peng J, et al. (2010) IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation. Cell Res 20(1):62-71 |
| abstractText | 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. |
