1. Volume 139, Issue 5, Pages 1448-1450 (November 2010)
Crohn's Disease Susceptibility Gene Interactions, a NOD to the Newcomer ATG16L1 
Ken Cadwell 
Gastroenterology 
Volume 139, Issue 5, Pages (November 2010)
DOI: /j.gastro
Copyright © 2010 AGA Institute Terms and Conditions

2. Figure 1
Mechanisms by which NOD2 and ATG16L1 functionally interact to control bacteria. All 3 of the following scenarios are disrupted by the Crohn's disease susceptibility alleles of NOD2 or ATG16L1. (A) NOD2 recruits ATG16L1 to the plasma membrane as bacteria enter the cell. Through ATG16L1, autophagy either targets bacteria in the cytosol or phagosomes to the lysosome for destruction. (B) NOD2 supports the recognition of MDP and mediates autophagy through RICK, NFκB, and ATG16L1. This enhanced autophagy leads to increased trafficking of MHC-II to the cell surface that allows a stronger T-cell response. (C) After exposure to MDP, NOD2 and RICK enhance 2 pathways downstream of ATG16L1, bacterial autophagy (as in A) and NFκB-mediated transcription. The crescent shaped vesicles depicted in these pathways represent nascent autophagosomes and/or associated autophagy proteins.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2010 AGA Institute Terms and Conditions