Department of Immunology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Cell Res. 2010 Jan;20(1):62-71. doi: 10.1038/cr.2009.128. Epub 2009 Nov 24.
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.
IL-23/IL-17 轴是各种炎症性疾病的重要调节剂。然而，IL-23 在过敏性气道炎症中的作用尚不清楚。在本研究中，我们表明在变应原诱导的哮喘模型中，过表达 IL-23R 的转基因小鼠表现出气道嗜酸性粒细胞浸润和 Th2 细胞因子产生增加，而 IL-23 缺乏的小鼠则表现出气道炎症减少。体外，IL-23-IL-23R 信号促进 GATA-3 表达并增强 Th2 细胞因子表达。相反，在没有这种信号的情况下，Th2 细胞分化被部分抑制。因此，IL-23 信号可能通过调节 Th2 细胞分化来调节过敏性哮喘。
