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Epidermal Growth Factor Receptor Expression Licenses Type-2 Helper T Cells to Function in a T Cell Receptor-Independent Fashion
Immunity ( IF 32.4 ) Pub Date : 2017-10-17 , DOI: 10.1016/j.immuni.2017.09.013
Carlos M Minutti 1 , Sebastian Drube 2 , Natalie Blair 1 , Christian Schwartz 3 , Jame C McCrae 1 , Andrew N McKenzie 4 , Thomas Kamradt 2 , Michal Mokry 5 , Paul J Coffer 5 , Maria Sibilia 6 , Alice J Sijts 7 , Padraic G Fallon 3 , Rick M Maizels 1 , Dietmar M Zaiss 1
Affiliation  

Gastro-intestinal helminth infections trigger the release of interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T cell receptor (TCR)-independent manner. Here, we show that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex between T1/ST2 (the IL-33R) and EGFR. This shared signaling complex allowed IL-33 to induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expression of IL-13. Lack of EGFR expression on T cells abrogated IL-13 expression in infected tissues and impaired host resistance. EGFR expression on Th2 cells was TCR-signaling dependent, and therefore, our data reveal a mechanism by which antigen presentation controls the innate effector function of Th2 cells at the site of inflammation.



中文翻译:

表皮生长因子受体表达允许 2 型辅助 T 细胞以 T 细胞受体独立方式发挥作用

胃肠蠕虫感染触发白细胞介素 33 (IL-33) 的释放,白细胞介素 33 (IL-33) 在感染部位诱导 2 型辅助 T 细胞 (Th2 细胞) 产生 IL-13,从而导致 T 细胞中的宿主抵抗力受体(TCR)非依赖性方式。在这里,我们表明,作为 IL-33 诱导的 IL-13 分泌的先决条件,Th2 细胞需要表皮生长因子受体 (EGFR) 及其配体双调蛋白的表达,才能在 T1 之间形成信号复合物。 /ST2 (IL-33R) 和 EGFR。这种共享的信号复合物允许 IL-33 诱导 EGFR 介导的 MAP 激酶信号通路的激活,从而诱导 IL-13 的表达。T 细胞上缺乏 EGFR 表达消除了感染组织中 IL-13 的表达并损害了宿主抵抗力。Th2 细胞上的 EGFR 表达依赖于 TCR 信号传导,

更新日期:2017-10-17
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