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淋病奈瑟菌通过 TGF-β 依赖的机制选择性地抑制 Th1 和 Th2 细胞的发育，并增强 Th17 细胞反应。

Neisseria gonorrhoeae selectively suppresses the development of Th1 and Th2 cells, and enhances Th17 cell responses, through TGF-β-dependent mechanisms.

机构信息

Department of Microbiology and Immunology, University at Buffalo, Buffalo, New York, USA.

出版信息

Mucosal Immunol. 2012 May;5(3):320-31. doi: 10.1038/mi.2012.12. Epub 2012 Feb 22.

DOI:10.1038/mi.2012.12
PMID:22354319
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3328619/
Abstract

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.

摘要

淋病奈瑟菌感染不会诱导特异性免疫或免疫记忆。我们之前在阴道淋病奈瑟菌感染的小鼠模型中的研究表明，由 Th17 细胞介导的先天免疫是该病原体引发的免疫反应的一个重要方面。在此，我们表明淋病奈瑟菌通过诱导 TGF-β选择性抑制 Th1 和 Th2 细胞，并促进 Th17 细胞的发育。虽然 Th17 反应取决于淋病奈瑟菌脂寡糖通过 TLR4 发挥作用，但淋病奈瑟菌对 Th1/Th2 反应的抑制作用涉及淋病奈瑟菌 Opa 蛋白。体外淋病奈瑟菌刺激的 Th17 反应可以通过阻断 TGF-β而不是阻断 IL-17 转向 Th1/Th2。研究结果表明，淋病奈瑟菌通过依赖 TGF-β的机制抑制 Th1/Th2 介导的适应性免疫反应，并且可以通过操纵这种作用来促进适应性免疫反应的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b5/3328619/f6177112c0b9/nihms352527f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b5/3328619/f33258c7c2be/nihms352527f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b5/3328619/e56bce0d5eeb/nihms352527f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b5/3328619/f6177112c0b9/nihms352527f7.jpg

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