IL-23 induces IL-22 and IL-17 production in response to Chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis.
IL-23 induces IL-22 and IL-17 production in response to Chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis.
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DOI：
10.1111/aji.12171
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发表时间：
2013-12
期刊：
影响因子：
--
通讯作者：
Darville T
中科院分区：
文献类型：
--
作者：
Frazer LC;Scurlock AM;Zurenski MA;Riley MM;Mintus M;Pociask DA;Sullivan JE;Andrews CW Jr;Darville T
沙眼衣原体感染是生殖道病理的重要原因。为了设计安全有效的疫苗，必须区分保护性和病理性免疫介质。将野生型小鼠和IL-22、IL-23缺失小鼠经阴道感染muridarum衣原体，比较其感染过程和输卵管病理变化。IL-23缺陷小鼠的局部生殖道和引流淋巴结免疫应答也被检测。IL-22和IL-23缺陷小鼠对感染和输卵管病理表现正常。在淋巴结中衣原体特异性Th17反应的发展以及生殖道中IL-22和IL-17的产生都需要IL-23。然而，在缺乏IL-23的情况下，Th1和先天免疫细胞的内流并未受到损害。在小鼠模型中，IL-22和IL-23在衣原体感染的发病机制中发挥多余或最小的作用。应避免衣原体疫苗诱导th17相关细胞因子，因为这些反应不是解决感染的核心，而且具有病理潜力。
Chlamydia trachomatis Infections are a significant cause of reproductive tract pathology. Protective and pathologic immune mediators must be differentiated in order to design a safe and effective vaccine. Wild-type mice and mice deficient in IL-22 and IL-23 were infected intravaginally with Chlamydia muridarum and their course of infection and oviduct pathology were compared. Local genital tract and draining lymph node immune responses were also examined in IL-23 deficient mice. IL-22 and IL-23 deficient mice exhibited normal susceptibility to infection and oviduct pathology. IL-23 was required for development of a Chlamydia-specific Th17 response in the lymph nodes and for production of IL-22 and IL-17 in the genital tract. However, influx of Th1 and innate immune cells was not compromised in the absence of IL-23. IL-22 and IL-23 play either redundant or minimal roles in the pathogenesis of Chlamydia infection in the mouse model. Induction of Th17-associated cytokines by a Chlamydia vaccine should be avoided since these responses are not central to resolution of infection and have pathologic potential.
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影响因子：
64.8
作者：
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影响因子：
5
作者：
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