Revisiting Crohn's disease as a primary immunodeficiency of macrophages

被引：106

作者：

Casanova, Jean-Laurent ^{[1
,2
]}

Abel, Laurent ^{[1
,2
]}

机构：

[1] Rockefeller Univ, Lab Human Genet Infect Dis, Rockefeller Branch, New York, NY 11065 USA

[2] Univ Paris 05, Lab Human Genet Infect Dis, Necker Branch, Inst Natl Rech & Sante Med,U550, Paris, France

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2009年 / 206卷 / 09期

关键词：

INFLAMMATORY-BOWEL-DISEASE; BACTERIAL-INFECTIONS; GENETIC DISSECTION; HUMAN IMMUNOLOGY; IMMUNITY; SUSCEPTIBILITY; MUTATIONS; ASSOCIATION; DYSFUNCTION; DEFICIENCY;

D O I：

10.1084/jem.20091683

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Despite two decades of mouse immunology and human genetics studies, the pathogenesis of Crohn's disease (CD) remains elusive. New clinical investigations suggest that CD may be caused by inborn errors of macrophages. These errors may result in impaired attraction of granulocytes to the gut wall, causing impaired clearance of intruding bacteria, thereby precipitating the formation of granulomas. This theory paves the way for a macrophage-based Mendelian genetic dissection of CD.

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页码：1839 / 1843

页数：5

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