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 1448-1450 (November 2010) DOI: 10.1053/j.gastro.2010.09.023 Copyright © 2010 AGA Institute Terms and Conditions

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 2010 139, 1448-1450DOI: (10.1053/j.gastro.2010.09.023) Copyright © 2010 AGA Institute Terms and Conditions