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首页> 美国卫生研究院文献>Infection and Immunity >Contribution of Interleukin-12 p35 (IL-12p35) and IL-12p40 to Protective Immunity and Pathology in Mice Infected with Chlamydia muridarum
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Contribution of Interleukin-12 p35 (IL-12p35) and IL-12p40 to Protective Immunity and Pathology in Mice Infected with Chlamydia muridarum

机译：白细胞介素12 p35（IL-12p35）和IL-12p40对感染衣原体的小鼠保护性免疫和病理的贡献。

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The p35 molecule is unique to interleukin-12 (IL-12), while p40 is shared by both IL-12 and IL-23. IL-12 promotes Th1 T cell responses, while IL-23 promotes Th17 T cell responses. The roles of IL-12p35- and IL-12p40-mediated responses in chlamydial infection were compared in mice following an intravaginal infection with Chlamydia muridarum. Mice deficient in either IL-12p35 or p40 both developed similar but prolonged infection time courses, confirming the roles of IL-12-mediated immune responses in clearing primary infection. However, all mice, regardless of genotype, cleared reinfection within 2 weeks, suggesting that an IL-12- or IL-23-independent adaptive immunity is protective against chlamydial infection. All infected mice developed severe oviduct hydrosalpinx despite the increased Th2 responses in IL-12p35- or IL-12p40-deficient mice, suggesting that Th2-dominant responses can contribute to Chlamydia-induced inflammatory pathology. Compared to IL-12p35 knockout mice, the IL-12p40-deficient mice exhibited more extensive spreading of chlamydial organisms into kidney tissues, leading to significantly increased incidence of pyelonephritis, which both confirms the role of IL-12 or IL-23-independent host responses in Chlamydia-induced pathologies and suggests that in the absence of IL-12/IFN-γ-mediated Th1 immunity, an IL-23-mediated response may play an important role in restricting chlamydial organisms from spreading into distal organs. These observations together provide important information for both understanding chlamydial pathogenesis and developing anti-Chlamydia vaccines.
机译：p35分子是白介素12（IL-12）独有的，而p40被IL-12和IL-23共有。 IL-12促进Th1 T细胞反应，而IL-23促进Th17 T细胞反应。在小鼠衣原体感染阴道后，比较了IL-12p35和IL-12p40介导的反应在衣原体感染中的作用。缺乏IL-12p35或p40的小鼠都发展出相似但延长的感染时间，从而证实了IL-12介导的免疫反应在清除原发感染中的作用。但是，所有小鼠，无论基因型如何，都在2周内清除了再次感染，这表明独立于IL-12或IL-23的适应性免疫对衣原体感染具有保护作用。尽管在IL-12p35或IL-12p40缺陷型小鼠中Th2反应增强，但所有感染的小鼠均发育出严重的输卵管输卵管积水，表明Th2阳性反应可有助于衣原体诱导的炎症病理。与敲除IL-12p35的小鼠相比，IL-12p40缺陷的小鼠表现出衣原体微生物更广泛地扩散到肾脏组织，导致肾盂肾炎的发病率显着增加，这都证实了IL-12或非IL-23独立宿主的作用衣原体诱导的病理学中的应答，表明在没有IL-12 /IFN-γ介导的Th1免疫的情况下，IL-23介导的应答可能在限制衣原体生物扩散到远端器官中起重要作用。这些观察结果为了解衣原体的发病机理和开发抗衣原体疫苗提供了重要的信息。

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