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首页> 外文期刊>Current opinion in gastroenterology >Flag in the crossroads: flagellin modulates innate and adaptive immunity.
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Flag in the crossroads: flagellin modulates innate and adaptive immunity.

机译：十字路口的标志物：鞭毛蛋白调节先天性和适应性免疫。

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PURPOSE OF REVIEW: To consider observations suggesting that the bacterial protein flagellin, the primary structural component of flagella, plays a major role in mediating gut inflammation associated with infection by enteric pathogens and in inflammatory bowel disease. RECENT FINDINGS: Biochemical dissection of an in-vitro model of bacterial-epithelial interactions revealed flagellin, via ligation of Toll-like receptor 5, to be a major means of activating the innate immune responses defining active intestinal inflammation. Application of the novel technique of serologic expression cloning to murine models of colitis discovered that flagellin is also a dominant target of the adaptive immune responses that drive colitis in such models. Human studies observed that flagellin was also a major antigenic target of immune responses associated with Crohn's disease. Carriers of dominant-negative Toll-like receptor 5 gene exhibit reduced natural acquisition of immunity to flagellin, indicating that the adaptive immune response to flagellin is likely driven, in part, by Toll-like receptor 5. In some genetic backgrounds dominant-negative Toll-like receptor 5 associated negatively with Crohn's disease, suggesting that immune responses to flagellin are not only associated with Crohn's disease, but can promote the pathogenic response. SUMMARY: Flagellin is a major activator of innate immunity thus driving pathogen-induced acute inflammation and, perhaps, the active flares of inflammatory bowel disease. Flagellin is also a dominant antigen of the Crohn's disease-associated adaptive immune response, thus placing this molecule at the crossroads of the innate and adaptive immune responses that are the hallmark of intestinal inflammation.
机译：审查目的：考虑观察结果，表明鞭毛的主要结构成分细菌鞭毛蛋白在介导与肠道病原体感染相关的肠道炎症和炎症性肠病中起着重要作用。最近的发现：细菌-上皮相互作用的体外模型的生化解剖显示，通过连接Toll样受体5，鞭毛蛋白是激活先天性免疫反应的主要手段，从而定义了活跃的肠道炎症。将血清学表达克隆的新技术应用到结肠炎的小鼠模型中，发现鞭毛蛋白也是在这种模型中驱动结肠炎的适应性免疫反应的主要靶标。人体研究发现，鞭毛蛋白还是与克罗恩氏病相关的免疫反应的主要抗原性靶标。显性负性Toll样受体5基因的携带者表现出降低的对鞭毛蛋白免疫的自然获得性，表明对鞭毛蛋白的适应性免疫反应可能部分由Toll样受体5驱动。在某些遗传背景下，显性负性Toll样受体5与克罗恩氏病呈负相关，这表明对鞭毛蛋白的免疫反应不仅与克罗恩病有关，而且可以促进病原性反应。简介：鞭毛蛋白是先天免疫的主要激活剂，因此可驱动病原体诱导的急性炎症，并可能引起炎症性肠病的活跃发作。鞭毛蛋白还是与克罗恩病相关的适应性免疫反应的主要抗原，因此使该分子处于先天性和适应性免疫反应的十字路口，后者是肠道炎症的标志。

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