Nod2-Dependent Regulation of Innate and Adaptive Immunity in the Intestinal Tract
Top Cited Papers
- 4 February 2005
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 307 (5710) , 731-734
- https://doi.org/10.1126/science.1104911
Abstract
The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.Keywords
This publication has 33 references indexed in Scilit:
- NOD2 (CARD15) mutations in Crohn's disease are associated with diminished mucosal -defensin expressionGut, 2004
- Regulation of IL-8 and IL-1 expression in Crohn's disease associated NOD2/CARD15 mutationsHuman Molecular Genetics, 2004
- Die Rolle der Defensine in der Pathogenese chronisch-entzündlicher DarmerkrankungenZeitschrift für Gastroenterologie, 2004
- Nod2 Is a General Sensor of Peptidoglycan through Muramyl Dipeptide (MDP) DetectionJournal of Biological Chemistry, 2003
- Host Recognition of Bacterial Muramyl Dipeptide Mediated through NOD2Journal of Biological Chemistry, 2003
- Induction of Nod2 in Myelomonocytic and Intestinal Epithelial Cells via Nuclear Factor-κB ActivationJournal of Biological Chemistry, 2002
- Small anti-viral compounds activate immune cells via the TLR7 MyD88–dependent signaling pathwayNature Immunology, 2002
- Nod2, a Nod1/Apaf-1 Family Member That Is Restricted to Monocytes and Activates NF-κBJournal of Biological Chemistry, 2001
- Regulation of Intestinal α-Defensin Activation by the Metalloproteinase Matrilysin in Innate Host DefenseScience, 1999
- Endotoxin-tolerant Mice Have Mutations in Toll-like Receptor 4 (Tlr4)The Journal of Experimental Medicine, 1999