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Paneth cells and innate mucosal immunity.

机译:Paneth细胞和先天黏膜免疫力。

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PURPOSE OF REVIEW: Recent evidence shows that disruption of Paneth cell homeostasis by induction of endoplasmic reticulum stress or autophagy, with consequent apoptosis, contributes to inflammation and morbidity in a variety of experimental mouse models. RECENT FINDINGS: Recent advances show that proinflammatory mediators in Paneth cell dense core secretory granules mediate tumor necrosis factor-alpha-induced shock, that Paneth cell alpha-defensins modulate the composition of the small intestinal microflora, that development of crypt organoid culture systems provides a novel means for investigating the crypt microenvironment, and that varied genetic defects that disrupt Paneth cell homeostasis are emergent as risk factors in inflammatory bowel disease. SUMMARY: This recent literature identifies Paneth cells as particularly sensitive targets of endoplasmic reticulum stress responses and implicates this unique small intestinal lineage in inflammatory bowel disease pathogenesis resulting from diverse heritable and environmental causes.
机译:审查目的:最近的证据表明,通过诱导内质网应激或自噬破坏Paneth细胞稳态,并随之导致细胞凋亡,在各种实验性小鼠模型中均引起炎症和发病。最近的发现:最近的进展表明,Paneth细胞致密核心分泌颗粒中的促炎性介质介导了肿瘤坏死因子-α引起的休克,Paneth细胞的α-防御素调节了小肠微生物群的组成,隐窝类器官培养系统的发展提供了一种研究隐窝微环境的新颖方法以及破坏Paneth细胞动态平衡的多种遗传缺陷已成为炎症性肠病的危险因素。简介:最近的文献将Paneth细胞鉴定为内质网应激反应的特别敏感目标,并将这种独特的小肠谱系牵涉到由多种遗传和环境原因引起的炎症性肠病发病机理中。

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