Immunologic regulation of toll-like receptors in gut epithelium
Immunologic regulation of toll-like receptors in gut epithelium
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DOI：
10.1097/00001574-200311000-00008
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发表时间：
2003-11-01
影响因子：
2.5
通讯作者：
Abreu, MT
中科院分区：
文献类型：
--
作者：
Abreu, MT
为了应对环境中病原体的存在，先天免疫系统已经进化到提供对微生物的快速防御。这种反应涉及通过一系列称为toll样受体的受体识别存在于不同微生物中的分子模式。本文的重点是在肠上皮细胞的toll样受体信号的调节。肠上皮细胞持续暴露于高浓度的各种细菌。尽管肠道细菌密度很高，但正常的肠道不会发炎。人类和动物的特发性炎症性肠病的特征是宿主与微生物的异常相互作用。最近的研究表明，肠上皮细胞对微生物产物的反应性很差。这种低反应性的原因是Toll样受体分子的表达减少或极化。炎症细胞因子上调toll样受体的表达。概述肠上皮细胞在微生物群的压力下进化，以抑制对肠道细菌的反应，同时保持对病原体的反应能力。在炎症性肠病中，对正常植物群的耐受性丧失可能部分是由于不适当的toll样受体信号传导。
Purpose of review In response to the presence of pathogens in the environment, the innate immune system has evolved to provide a rapid defense against microbes. This response involves the recognition of molecular patterns present in diverse microbes by a series of receptors termed toll-like receptors. The focus of this article is the regulation of toll-like receptor signaling in the intestinal epithelium. The intestinal epithelium is continually exposed to a high concentration of diverse bacteria. In spite of the density of commensal bacteria, the normal intestine is not inflamed. Idiopathic inflammatory bowel disease in humans and animals is characterized by aberrant host-microbial interactions.Recent findings Several studies demonstrate that intestinal epithelial cells are poorly responsive to microbial products. The reason for this hyporesponsiveness is decreased or polarized expression of toll-like receptor molecules. Inflammatory cytokines upregulate expression of toll-like receptors.Summary The intestinal epithelium has evolved under the pressure of the microbiota to mute a response to commensal bacteria while maintaining the ability to respond to pathogens. In inflammatory bowel disease, the loss of tolerance to the normal flora may be due in part to inappropriate toll-like receptor signaling.