Intestinal homeostasis and its breakdown in inflammatory bowel disease

被引:1491
|
作者
Maloy, Kevin J. [1 ]
Powrie, Fiona [1 ,2 ]
机构
[1] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England
[2] Univ Oxford, John Radcliffe Hosp, Expt Med Div NDM, Translat Gastroenterol Unit, Oxford OX3 9DU, England
基金
英国惠康基金;
关键词
REGULATORY T-CELLS; GROWTH-FACTOR-BETA; DENDRITIC CELLS; TRANSCRIPTION FACTOR; MAINTAIN HOMEOSTASIS; IMMUNE-RESPONSES; EPITHELIAL-CELLS; GUT MICROBIOTA; GENE ATG16L1; MOUSE MODELS;
D O I
10.1038/nature10208
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Intestinal homeostasis depends on complex interactions between the microbiota, the intestinal epithelium and the host immune system. Diverse regulatory mechanisms cooperate to maintain intestinal homeostasis, and a breakdown in these pathways may precipitate the chronic inflammatory pathology found in inflammatory bowel disease. It is now evident that immune effector modules that drive intestinal inflammation are conserved across innate and adaptive leukocytes and can be controlled by host regulatory cells. Recent evidence suggests that several factors may tip the balance between homeostasis and intestinal inflammation, presenting future challenges for the development of new therapies for inflammatory bowel disease.
引用
收藏
页码:298 / 306
页数:9
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