The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Chinese Academy of Sciences & Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nat Immunol. 2011 Oct 12;12(12):1151-8. doi: 10.1038/ni.2155.
Interleukin 17 receptor E (IL-17RE) is an orphan receptor of the IL-17 receptor family. Here we show that IL-17RE is a receptor specific to IL-17C and has an essential role in host mucosal defense against infection. IL-17C activated downstream signaling through IL-17RE-IL-17RA complex for the induction of genes encoding antibacterial peptides as well as proinflammatory molecules. IL-17C was upregulated in colon epithelial cells during infection with Citrobacter rodentium and acted in synergy with IL-22 to induce the expression of antibacterial peptides in colon epithelial cells. Loss of IL-17C-mediated signaling in IL-17RE-deficient mice led to lower expression of genes encoding antibacterial molecules, greater bacterial burden and early mortality during infection. Together our data identify IL-17RE as a receptor of IL-17C that regulates early innate immunity to intestinal pathogens.
白细胞介素 17 受体 E（IL-17RE）是白细胞介素 17 受体家族的孤儿受体。在这里，我们表明 IL-17RE 是一种专门针对 IL-17C 的受体，在宿主黏膜防御感染方面发挥着重要作用。IL-17C 通过 IL-17RE-IL-17RA 复合物激活下游信号通路，诱导编码抗菌肽和促炎分子的基因表达。在感染柠檬酸杆菌时，IL-17C 在结肠上皮细胞中上调，并与 IL-22 协同作用，诱导结肠上皮细胞中抗菌肽的表达。在缺乏 IL-17C 介导的信号转导的 IL-17RE 缺陷小鼠中，编码抗菌分子的基因表达降低，感染期间细菌负荷增加，早期死亡率增加。总之，我们的数据将 IL-17RE 鉴定为 IL-17C 的受体，该受体调节对肠道病原体的早期先天免疫。
