Neisseria gonorrhoeae selectively suppresses the development of Th1 and Th2 cells, and enhances Th17 cell responses, through TGF-β-dependent mechanisms
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 th...
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Published in | Mucosal immunology Vol. 5; no. 3; pp. 320 - 331 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Nature Publishing Group US
01.05.2012
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1933-0219 1935-3456 |
DOI: | 10.1038/mi.2012.12 |