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首页> 外文期刊>Infection and immunity >Ecto-5′-Nucleotidase (CD73) Deficiency in Mycobacterium tuberculosis-Infected Mice Enhances Neutrophil Recruitment
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Ecto-5′-Nucleotidase (CD73) Deficiency in Mycobacterium tuberculosis-Infected Mice Enhances Neutrophil Recruitment

机译：结核分枝杆菌感染小鼠中的Ecto-5'-核苷酸酶（CD73）缺乏会增强中性粒细胞的招募。

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The immune system needs safeguards that prevent collateral tissue damage mediated by the immune system while enabling an effective response against a pathogen. The purinergic pathway is one such mechanism and finely modulates inflammation by sensing nucleotides in the environment. Extracellular ATP is considered to be a danger signal leading to a proinflammatory response, whereas adenosine is immunosuppressive. CD73, also called ecto-5′-nucleotidase, occupies a strategic position in this pathway, as it is the main enzyme responsible for the generation of adenosine from ATP. Here, we explore the role of CD73 during tuberculosis, a disease characterized by an immune response that is harmful to the host and unable to eradicate Mycobacterium tuberculosis. Using CD73 knockout (KO) mice, we found that CD73 regulates the response to M. tuberculosis infection in vitro and in vivo. Mycobacterium-infected murine macrophages derived from CD73 KO mice secrete more keratinocyte chemoattractant (KC), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) and release less vascular endothelial growth factor (VEGF) upon ATP stimulation than do those derived from wild-type (WT) mice. In vivo, CD73 limits the early influx of neutrophils to the lungs without affecting bacterial growth and dissemination. Collectively, our results support the view that CD73 fine-tunes antimycobacterial immune responses.
机译：免疫系统需要安全防护措施，以防止由免疫系统介导的附带组织损害，同时能够有效应对病原体。嘌呤能途径就是这样一种机制，并且通过感测环境中的核苷酸来精细地调节炎症。细胞外ATP被认为是导致促炎反应的危险信号，而腺苷具有免疫抑制作用。 CD73，也称为ecto-5'-核苷酸酶，在该途径中占有重要地位，因为它是负责从ATP产生腺苷的主要酶。在这里，我们探讨了CD73在结核病中的作用，结核病是一种以免疫反应为特征的疾病，对宿主有害，无法根除结核分枝杆菌。使用CD73基因敲除（KO）小鼠，我们发现CD73在体外和体内调节对结核分枝杆菌感染的反应。来自CD73 KO小鼠的分枝杆菌感染的鼠巨噬细胞分泌更多的角质形成细胞趋化因子（KC），肿瘤坏死因子α（TNF-α）和白介素6（IL-6），并在ATP刺激下释放较少的血管内皮生长因子（VEGF）比那些衍生自野生型（WT）的小鼠要高。在体内，CD73限制了中性粒细胞向肺的早期流入，而不会影响细菌的生长和传播。总的来说，我们的结果支持CD73可以微调抗分枝杆菌免疫反应的观点。

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