Format

Send to

Choose Destination
Trends Mol Med. 2005 Jul;11(7):307-9.

NOD2 mutation and mice: no Crohn's disease but many lessons to learn.

Author information

1
University of California-Davis School of Medicine, Department of Microbiology and Immunology, 1 Shield Avenue, Tupper Hall 3146, Davis, CA 95616, USA. jwehkamp@ucdavis.edu

Abstract

Many patients with ileal Crohn's disease, a chronic intestinal inflammation, carry mutations in the gene encoding NOD2 (CARD15), but the mechanistic details of how this mutation leads to disease are not fully understood. NOD2 is expressed in antigen-presenting cells and Paneth cells, which are secretory epithelial cells of the small intestine. Two complementary studies using genetically engineered murine models help to explain the association of NOD2 malfunction and mucosal disease. One study observes a dysregulation of proinflammatory responses, suggesting that the most common NOD2 mutation in humans results in a gain of function. The other study determined that NOD2-null mutations impair the Paneth-cell antimicrobial response, which is consistent with recent findings in humans. Together, these studies fuel optimism that new therapeutic directions might emerge to better treat this severe mucosal disease.

PMID:
15955743
DOI:
10.1016/j.molmed.2005.06.003
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center