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首页> 外文期刊>Current opinion in gastroenterology >Nucleotide-binding-oligomerization domain proteins and toll-like receptors: sensors of the inflammatory bowel diseases' microbial environment.
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Nucleotide-binding-oligomerization domain proteins and toll-like receptors: sensors of the inflammatory bowel diseases' microbial environment.

机译:核苷酸结合寡聚域蛋白和toll样受体:炎性肠病微生物环境的传感器。

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摘要

PURPOSE OF REVIEW: Chronic inflammatory bowel diseases appear to result from inappropriate immune responses driven by apparently normal intestinal microflora in genetically susceptible hosts. This review focuses on recently described mechanisms balancing toll-like receptor and nucleotide-binding-oligomerization domain activation in the face of ubiquitous enteric flora. RECENT FINDINGS: Toll-like receptor and nucleotide-binding-oligomerization domain signaling plays an integral role in the close collaboration between the intestinal epithelial cell monolayer and adjacent mucosal immune cells. Pathways activated by functional cytosolic nucleotide-binding-oligomerization domain proteins appear to interact with those mediated by membrane-associated toll-like receptors in the innate and adaptive immune defense against intra-and extracellular pathogens. Nucleotide-binding-oligomerization domain-mediated signaling may also control toll-like receptor-induced proinflammatory pathways. SUMMARY: Intersections between toll-like receptor and nucleotide-binding-oligomerization domain pathways may exist to refine the host immune response to pathogens and prevent undesired immune stimulation driven by the intestinal microbiota. Deficient toll-like receptor and nucleotide-binding-oligomerization domain function due to genetic variability is associated with an increased susceptibility to the development of inflammatory bowel disease.
机译:审查目的:慢性炎症性肠病似乎是由于遗传易感宿主中明显正常的肠道菌群驱动的不适当的免疫反应所致。这篇综述集中在最近描述的机制上,该机制在面对普遍存在的肠道菌群时,平衡了收费型受体和核苷酸结合-寡聚域的激活。最近的发现:Toll样受体和核苷酸结合寡聚域信号传导在肠上皮细胞单层细胞和邻近的粘膜免疫细胞之间的紧密协作中起着不可或缺的作用。功能性胞质核苷酸结合-寡聚化域蛋白激活的途径似乎与膜相关的toll样受体介导的那些相互作用,对先天性和适应性免疫防御细胞内和细胞外病原体。核苷酸结合-寡聚化域介导的信号转导也可能控制收费样受体诱导的促炎途径。摘要:Toll样受体和核苷酸结合-寡聚化域途径之间可能存在交叉点,以改善宿主对病原体的免疫反应并防止肠道菌群驱动的不良免疫刺激。由于遗传变异而导致的toll样受体和核苷酸结合寡聚域功能不足,与炎症性肠病的易感性增加有关。

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