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本文引用的文献

1
Intestinal mucosal barrier function in health and disease.健康与疾病状态下的肠道黏膜屏障功能
Nat Rev Immunol. 2009 Nov;9(11):799-809. doi: 10.1038/nri2653.
2
The multifaceted influence of the mucosal microflora on mucosal dendritic cell responses.黏膜微生物群对黏膜树突状细胞反应的多方面影响。
Immunity. 2009 Sep 18;31(3):377-88. doi: 10.1016/j.immuni.2009.09.001.
3
Immune responses to the microbiota at the intestinal mucosal surface.肠道黏膜表面对微生物群的免疫反应。
Immunity. 2009 Sep 18;31(3):368-76. doi: 10.1016/j.immuni.2009.08.009.
4
Defect in CEACAM family member expression in Crohn's disease IECs is regulated by the transcription factor SOX9.CEACAM 家族成员在克罗恩病 IEC 中的表达缺陷受转录因子 SOX9 调控。
Inflamm Bowel Dis. 2009 Dec;15(12):1775-83. doi: 10.1002/ibd.21023. Epub 2009 Jul 27.
5
Intestinal barrier function: molecular regulation and disease pathogenesis.肠道屏障功能:分子调控与疾病发病机制
J Allergy Clin Immunol. 2009 Jul;124(1):3-20; quiz 21-2. doi: 10.1016/j.jaci.2009.05.038.
6
Lymphoepithelial interactions: a new paradigm.淋巴细胞与上皮细胞的相互作用:一种新范式。
Ann N Y Acad Sci. 2009 May;1165:323-6. doi: 10.1111/j.1749-6632.2009.04061.x.
7
Epithelial tight junctions in intestinal inflammation.肠道炎症中的上皮紧密连接
Ann N Y Acad Sci. 2009 May;1165:294-300. doi: 10.1111/j.1749-6632.2009.04062.x.
8
Colitis-associated variant of TLR2 causes impaired mucosal repair because of TFF3 deficiency.由于三叶因子3(TFF3)缺乏,TLR2的结肠炎相关变体导致黏膜修复受损。
Gastroenterology. 2009 Jul;137(1):209-20. doi: 10.1053/j.gastro.2009.03.007. Epub 2009 Mar 18.
9
Defensins and inflammation: the role of defensins in inflammatory bowel disease.防御素与炎症:防御素在炎症性肠病中的作用
J Gastroenterol Hepatol. 2009 Feb;24(2):202-8. doi: 10.1111/j.1440-1746.2008.05772.x.
10
The molecular basis of NOD2 susceptibility mutations in Crohn's disease.克罗恩病中NOD2易感性突变的分子基础。
Mucosal Immunol. 2008 Nov;1 Suppl 1(0 1):S5-9. doi: 10.1038/mi.2008.42.

炎症性肠病中的肠上皮细胞。

Intestinal epithelial cells in inflammatory bowel diseases.

机构信息

Department of Clinical Medicine, University of Bologna, Gastroenterology Unit, S. Orsola - Malpighi Hospital, 40138 Bologna, Italy.

出版信息

World J Gastroenterol. 2010 Sep 14;16(34):4264-71. doi: 10.3748/wjg.v16.i34.4264.

DOI:10.3748/wjg.v16.i34.4264
PMID:20818809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2937106/
Abstract

The pathogenesis of inflammatory bowel diseases (IBDs) seems to involve a primary defect in one or more of the elements responsible for the maintenance of intestinal homeostasis and oral tolerance. The most important element is represented by the intestinal barrier, a complex system formed mostly by intestinal epithelial cells (IECs). IECs have an active role in producing mucus and regulating its composition; they provide a physical barrier capable of controlling antigen traffic through the intestinal mucosa. At the same time, they are able to play the role of non-professional antigen presenting cells, by processing and presenting antigens directly to the cells of the intestinal immune system. On the other hand, immune cells regulate epithelial growth and differentiation, producing a continuous bi-directional cross-talk within the barrier. Several alterations of the barrier function have been identified in IBD, starting from mucus features up to its components, from epithelial junctions up to the Toll-like receptors, and altered immune responses. It remains to be understood whether these defects are primary causes of epithelial damage or secondary effects. We review the possible role of the epithelial barrier and particularly describe the role of IECs in the pathogenesis of IBD.

摘要

炎症性肠病(IBD)的发病机制似乎涉及负责维持肠道内稳态和口服耐受的一个或多个元素的主要缺陷。最重要的元素是肠道屏障,这是一个主要由肠上皮细胞(IEC)组成的复杂系统。IEC 在产生粘液和调节其组成方面发挥着积极作用;它们提供了一个物理屏障,能够控制抗原通过肠黏膜的运输。同时,它们能够作为非专业抗原呈递细胞,直接将抗原加工和呈递给肠道免疫系统的细胞。另一方面,免疫细胞调节上皮细胞的生长和分化,在屏障内产生持续的双向细胞间交流。在 IBD 中已经确定了几种屏障功能的改变,从粘液特征到其成分,从上皮连接到 Toll 样受体,以及改变的免疫反应。尚不清楚这些缺陷是上皮损伤的主要原因还是次要影响。我们综述了上皮屏障的可能作用,并特别描述了 IEC 在 IBD 发病机制中的作用。