IL-17RE is the functional receptor for IL-17C and mediates mucosal immunity to infection with intestinal pathogens

被引：253

作者：

Song, Xinyang ^{[1
,2
]}

Zhu, Shu ^{[1
,2
]}

Shi, Peiqing ^{[1
,2
]}

Liu, Yan ^{[1
,2
]}

Shi, Yufang ^{[1
,2
]}

Levin, Steven D. ^{[3
]}

Qian, Youcun ^{[1
,2
]}

机构：

[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China

[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai 200030, Peoples R China

[3] ZymoGenetics, Dept Immunol, Seattle, WA USA

来源：

NATURE IMMUNOLOGY | 2011年 / 12卷 / 12期

基金：

中国国家自然科学基金;

关键词：

HOST-DEFENSE; INTERLEUKIN-17; RECEPTOR; IDENTIFICATION; EXPRESSION; AUTOIMMUNE; CYTOKINES; CELLS; ACT1; REQUIREMENT; SUPPRESSION;

D O I：

10.1038/ni.2155

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：1151 / U

页数：9

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