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首页> 外文期刊>Mucosal immunology >Neisseria gonorrhoeae selectively suppresses the development of Th1 and Th2 cells, and enhances Th17 cell responses, through TGF-β-dependent mechanisms
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Neisseria gonorrhoeae selectively suppresses the development of Th1 and Th2 cells, and enhances Th17 cell responses, through TGF-β-dependent mechanisms

机译：淋病奈瑟菌通过TGF-β依赖性机制选择性抑制Th1和Th2细胞的发育并增强Th17细胞反应

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摘要

Infection with Neisseria gonorrhoeae does not induce specific immunity or immune memory. Our previous studies in a murine model of vaginal gonococcal infection showed that innate immunity governed by Th17 cells was a critical aspect of the immune response elicited by this pathogen. Herein we show that N. gonorrhoeae selectively inhibited Th1 and Th2 cells and enhanced Th17 cell development through the induction of TGF-β. Whereas Th17 responses depended on gonococcal lipooligosaccharide acting through TLR4, the inhibitory effect of N. gonorrhoeae on Th1/Th2 responses involved gonococcal Opa proteins. In vitro Th17 responses to N. gonorrhoeae could be diverted to Th1/Th2 by blockade of TGF-β, but not by blockade of IL-17. The results reveal that N. gonorrhoeae suppresses Th1/Th2-mediated adaptive immune response through mechanisms dependent on TGF-β, and that this effect can be manipulated to promote the development of adaptive immunity.
机译：淋病奈瑟氏球菌感染不会诱导特异性免疫或免疫记忆。我们先前在小鼠阴道淋球菌感染模型中进行的研究表明，由Th17细胞控制的先天免疫是这种病原体引发的免疫反应的关键方面。在这里，我们表明淋病奈瑟氏球菌通过诱导TGF-β选择性抑制Th1和Th2细胞并增强Th17细胞发育。 Th17应答依赖于通过TLR4起作用的淋球菌脂寡糖，而淋病奈瑟菌对Th1 / Th2应答的抑制作用涉及淋球菌Opa蛋白。体外对淋病奈瑟菌的Th17反应可通过阻断TGF-β转移至Th1 / Th2，但不能通过阻断IL-17转移至Th1 / Th2。结果表明淋病奈瑟氏球菌通过依赖于TGF-β的机制抑制Th1 / Th2介导的适应性免疫反应，并且可以操纵这种作用以促进适应性免疫的发展。

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