4.8 Article

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

期刊

CELL RESEARCH
卷 20, 期 1, 页码 62-71

出版社

INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2009.128

关键词

cytokines; helper T cells; T cell differentiation; allergic airway inflammation

资金

  1. NIH
  2. MD Anderson Center for Targeted Therapy
  3. American Heart Association
  4. Ministry of Education of China
  5. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI071130] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR050772] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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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