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

被引：69
|
作者：
Liu, Y. [1 ,2 ]
Islam, E. A. [3 ]
Jarvis, G. A. [4 ,5 ]
Gray-Owen, S. D. [3 ]
Russell, M. W. [1 ,2 ]
机构：
[1] SUNY Buffalo, Dept Microbiol & Immunol, Buffalo, NY 14260 USA
[2] SUNY Buffalo, Witebsky Ctr Microbial Pathogenesis & Immunol, Buffalo, NY 14260 USA
[3] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada
[4] Vet Affairs Med Ctr, Ctr Immunochem, San Francisco, CA 94121 USA
[5] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
来源：
MUCOSAL IMMUNOLOGY | 2012年 / 5卷 / 03期
基金：
加拿大健康研究院;
关键词：
OPACITY PROTEIN EXPRESSION; GENITAL-TRACT; ANTIBODY-RESPONSES; ADAPTIVE IMMUNITY; SERUM RESISTANCE; OPA PROTEINS; ACTIVATION; INFECTION; ADHESION; BINDING;
D O I：
10.1038/mi.2012.12
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
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-beta. 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-beta, 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-beta, and that this effect can be manipulated to promote the development of adaptive immunity.
引用
收藏
页码：320 / 331
页数：12
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