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炎症性肠病:遗传学与固有免疫的最新进展

Inflammatory bowel disease: recent advances on genetics and innate immunity.

作者信息

Karantanos Theodoros, Gazouli Maria

机构信息

Department of Biology, School of Medicine, University of Athens, Greece.

出版信息

Ann Gastroenterol. 2011;24(3):164-172.

PMID:24713780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3959308/
Abstract

The chronic inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are recognized as important causes of gastrointestinal disease in children and adults. Insight into IBD is advancing rapidly owing to a plethora of investigations into intestinal inflammation in animal models, advances in the interrogation of diseases inherited as complex genetic traits, and the development of methods to define the composition of the intestinal microbiota. These advances offer a better understanding of the genetically determined interplay between the commensal microbiota, intestinal cells and the immune system, and the manner in which this interaction might be modified by environmental factors in the pathogenesis of IBD. The present review highlights recent advances in IBD research.

摘要

慢性炎症性肠病(IBD),即克罗恩病和溃疡性结肠炎,被认为是儿童和成人胃肠道疾病的重要病因。由于对动物模型肠道炎症进行了大量研究、在对作为复杂遗传性状遗传的疾病的探究方面取得进展以及确定肠道微生物群组成的方法的发展,对IBD的认识正在迅速推进。这些进展有助于更好地理解共生微生物群、肠道细胞和免疫系统之间由基因决定的相互作用,以及在IBD发病机制中这种相互作用可能如何被环境因素改变。本综述重点介绍了IBD研究的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/621f51cdc620/AnnGastroenterol-24-164-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/df0666e6c2ca/AnnGastroenterol-24-164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/b77fdb6f92a8/AnnGastroenterol-24-164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/621f51cdc620/AnnGastroenterol-24-164-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/df0666e6c2ca/AnnGastroenterol-24-164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/b77fdb6f92a8/AnnGastroenterol-24-164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a7c/3959308/621f51cdc620/AnnGastroenterol-24-164-g003.jpg

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本文引用的文献

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MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18.MyD88 介导的信号通路可预防结肠腺癌的发生:白介素 18 的作用。
J Exp Med. 2010 Aug 2;207(8):1625-36. doi: 10.1084/jem.20100199. Epub 2010 Jul 12.
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The NLRP3 inflammasome functions as a negative regulator of tumorigenesis during colitis-associated cancer.NLRP3 炎性小体在结肠炎相关癌症中作为肿瘤发生的负调节因子发挥作用。
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NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation.
Circulating circular RNA_103516 levels are increased in adult patients with inflammatory bowel disease and may serve as a novel biomarker.
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Mast Cells Exert Anti-Inflammatory Effects in an IL10 Model of Spontaneous Colitis.肥大细胞在 IL10 模型自发性结肠炎中发挥抗炎作用。
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Innate immunity includes defensins.固有免疫包括防御素。
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Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry.Nod1 和 Nod2 通过将 ATG16L1 招募到细菌进入部位的质膜上来指导自噬。
Nat Immunol. 2010 Jan;11(1):55-62. doi: 10.1038/ni.1823. Epub 2009 Nov 8.
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Inflammatory bowel disease and mutations affecting the interleukin-10 receptor.炎症性肠病与影响白细胞介素-10受体的突变
N Engl J Med. 2009 Nov 19;361(21):2033-45. doi: 10.1056/NEJMoa0907206. Epub 2009 Nov 4.
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Mucosal Immunol. 2010 Jan;3(1):11-6. doi: 10.1038/mi.2009.122. Epub 2009 Oct 28.
7
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