Critical role of Th17 responses in a murine model of Neisseria gonorrhoeae genital infection.

Critical role of Th17 responses in a murine model of Neisseria gonorrhoeae genital infection.
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DOI:
10.1038/mi.2009.139
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发表时间:
2010-05
期刊:
影响因子:
8
通讯作者:
--
中科院分区:
医学1区
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--
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Host immune responses, including the characteristic influx of neutrophils, against Neisseria gonorrhoeae are poorly understood; adaptive immunity is minimal and nonprotective. We hypothesize that N. gonorrhoeae selectively elicits Th17-dependent responses which recruit innate defense mechanisms including neutrophils and antimicrobial proteins that it can resist. We found that N. gonorrhoeae induced production of IL-17 in mouse T cells and of Th17-inducing cytokines in mouse and human antigen-presenting cells in vitro. IL-17 was induced in the iliac lymph nodes in vivo in a female mouse model of genital tract gonococcal infection. Antibody blockade of IL-17 or deletion of the major IL-17 receptor in IL-17RA-knockoutmice led to prolonged infection and diminished neutrophil influx. Genital tract tissue from IL-17RA-knockout mice showed reduced production of neutrophil-attractant chemokines in response to culture with N. gonorrhoeae. These results imply a crucial role for IL-17 and Th17 cells in the immune response to N. gonorrhoeae.
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