期刊
MUCOSAL IMMUNOLOGY
卷 7, 期 1, 页码 165-176出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2013.36
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资金
- NIH [AI074791]
- National Institute of Allergy and Infectious Diseases
- John R. Oishei Foundation, Buffalo, NY, USA
Infection with Neisseria gonorrhoeae triggers an intense inflammatory response characterized by an influx of neutrophils in the genital tract, yet natural gonococcal infection does not induce a state of protective immunity. Our previous studies in a mouse model of N. gonorrhoeae infection demonstrated that transforming growth factor-beta (TGF-beta) is involved in the suppression of adaptive immunity by this organism, but complete inhibition of TGF-beta activity only partially reverses N. gonorrhoeae-mediated suppression of T helper type 1 (Th1) and Th2 responses. In this study, we show that N. gonorrhoeae strongly induced the production of interleukin (IL)-10 and type 1 regulatory T (Tr1) cells. Blockade of IL-10 and Tr1 cell activity enhanced both Th1/Th2-dependent adaptive immune responses and Th17-governed innate responses to N. gonorrhoeae. Treatment of mice with anti-IL-10 antibody during gonococcal challenge led to faster clearance of infection and induced protection against secondary infection, with the generation of circulating and vaginal anti-gonococcal antibodies. Our results suggest that inhibition of IL-10 and Tr1 cells affords a new approach to the treatment of gonorrhea and facilitates the development of specific protective immunity.
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