Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
J Immunol. 2010 Mar 15;184(6):3186-90. doi: 10.4049/jimmunol.0901860. Epub 2010 Feb 10.
IL-4 promotes the development of Th2 cells and allergic inflammation. In atopic dermatitis lesions, IL-4 decreases the expression of multiple genes associated with innate defense, including genes in the epidermal differentiation complex (EDC) that regulate epidermal barrier function. However, it is not clear whether IL-4 also contributes to homeostatic control of EDC genes. In this report, we demonstrate that expression of EDC genes and barrier function is increased in the absence of endogenous IL-4. Mice that express a constitutively active Stat6 (Stat6VT) are prone to the development of allergic skin inflammation and have decreased expression of EDC genes. IL-4 deficiency protects Stat6VT transgenic mice from the development of allergic skin inflammation and decreased recovery time in barrier function following skin irritation, with a concomitant increase in EDC gene expression. These data suggest that IL-4 plays an important role in regulating epidermal homeostasis and innate barrier function.
IL-4 促进 Th2 细胞的发育和过敏炎症。在特应性皮炎病变中，IL-4 降低了与先天防御相关的多个基因的表达，包括调节表皮屏障功能的表皮分化复合物（EDC）中的基因。然而，目前尚不清楚 IL-4 是否也有助于 EDC 基因的稳态控制。在本报告中，我们证明了在没有内源性 IL-4 的情况下，EDC 基因的表达和屏障功能增加。表达组成型激活 Stat6（Stat6VT）的小鼠易发生过敏皮肤炎症，并且 EDC 基因的表达降低。IL-4 缺乏可防止 Stat6VT 转基因小鼠发生过敏皮肤炎症，并在皮肤刺激后屏障功能恢复时间缩短，同时 EDC 基因表达增加。这些数据表明，IL-4 在调节表皮稳态和先天屏障功能方面发挥着重要作用。
