Type III effectors of Enteroopathogenic Escherichia coli (EPEC) regulate the host immunity.

肠致病性大肠杆菌（EPEC）和啮齿类柠檬酸杆菌（C.啮齿类）分别在人和小鼠中引起严重的结肠炎。这些细菌具有III型分泌系统（TTSS）来调节感染。尽管已有报道表明一些III型效应子调节先天免疫应答，但TTSS是否调节宿主的适应性免疫仍不清楚。本实验主要研究了细菌TTSS对宿主获得性免疫的调节作用，结果发现细菌TTSS在体内外均可诱导Th 2细胞分化。TTSS通过抑制IL-12和IL-27等Th 1细胞因子诱导Th 2细胞分化。此外，Th 2细胞因子增强体内细菌感染。在本研究中，我们发现，EPEC和C。TTSS通过调节宿主的适应性免疫和诱导Th 2细胞分化来增强毒力。

Enteropathogenic Escherichia coli (EPEC) and Citrobacter rodentium (C. rodentium) cause severe colitis in human and mouse respectively. These bacteria have type III secretion system (TTSS) to regulate the infection. Although it has been reported that some type III effectors regulate innate immune responses, it is still unclear whether TTSS regulates the host adaptive immunity. Here, we focused on the regulation of host adaptive immunity by bacterial TTSS.As a result, we found that these bacteria induced Th2 differentiation by TTSS in vivo and in vitro. And this Th2 differentiation was induced by inhibition of Th1 cytokines such as IL-12 and IL-27 by TTSS. Furthermore, Th2 cytokines enhanced bacterial infection in vivo. In this study, we revealed that EPEC and C. rodentium regulated host adaptive immunity and Th2 differentiation was induced by TTSS in order to enhance their virulence.