Genetics and pathogenesis of inflammatory bowel disease

被引：1853

作者：

Khor, Bernard ^{[1
,2
,3
,4
]}

Gardet, Agnes ^{[1
,2
,3
]}

Xavier, Ramnik J. ^{[1
,2
,3
,5
]}

机构：

[1] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA

[2] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA

[3] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA

[4] Massachusetts Gen Hosp, Pathol Serv, Boston, MA 02114 USA

[5] Broad Inst MIT & Harvard, Cambridge Ctr 7, Cambridge, MA 02142 USA

来源：

NATURE | 2011年 / 474卷 / 7351期

基金：

美国国家卫生研究院;

关键词：

GENOME-WIDE ASSOCIATION; REGULATORY T-CELLS; INTESTINAL HOMEOSTASIS; TRANSCRIPTION FACTOR; SUSCEPTIBILITY LOCI; INDUCED COLITIS; GUT MICROBIOTA; CROHN-DISEASE; KEY ROLE; PROTEIN;

D O I：

10.1038/nature10209

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：

Recent advances have provided substantial insight into the maintenance of mucosal immunity and the pathogenesis of inflammatory bowel disease. Cellular programs responsible for intestinal homeostasis use diverse intracellular and intercellular networks to promote immune tolerance, inflammation or epithelial restitution. Complex interfaces integrate local host and microbial signals to activate appropriate effector programs selectively and even drive plasticity between these programs. In addition, genetic studies and mouse models have emphasized the role of genetic predispositions and how they affect interactions with microbial and environmental factors, leading to pro-colitogenic perturbations of the host-commensal relationship.

引用

页码：307 / 317

页数：11

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