NOD2-mediated autophagy and Crohn disease.

Autophagy is important in immune cells as a means of disposing of pathogens and in connecting with the antigen presentation machinery to facilitate immune priming and initiation of a correctly targeted adaptive immune response. While Toll-like receptors (TLRs) are known to regulate autophagy in this...

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Main Authors: Brain, O, Allan, P, Simmons, A
Format: Journal article
Language:English
Published: 2010
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author Brain, O
Allan, P
Simmons, A
author_facet Brain, O
Allan, P
Simmons, A
author_sort Brain, O
collection OXFORD
description Autophagy is important in immune cells as a means of disposing of pathogens and in connecting with the antigen presentation machinery to facilitate immune priming and initiation of a correctly targeted adaptive immune response. While Toll-like receptors (TLRs) are known to regulate autophagy in this context, the extent to which other pattern recognition receptors (PRRs) are involved has been unclear. NOD2 is an intracellular PRR of the Nod-like receptor (NLR) family that is notable in that variants in the ligand recognition domain are associated with Crohn disease (CD). Our recent study shows NOD2 activates autophagy in a manner requiring ATG16L1, another CD susceptibility gene. NOD2 autophagy induction is required for bacterial handling and MHC class II antigen presentation in human dendritic cells (DCs). CD patients DCs expressing CD risk variant NOD2 or ATG16L1 display reduced autophagy induction after NOD2 triggering resulting in reduced bacterial killing and defective antigen presentation. Aberrant bacterial handling and immune priming could act as a trigger for inflammation in CD.
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spelling oxford-uuid:7af79032-7904-4fe8-95b8-c11e5fa6d5702022-03-26T20:47:30ZNOD2-mediated autophagy and Crohn disease.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:7af79032-7904-4fe8-95b8-c11e5fa6d570EnglishSymplectic Elements at Oxford2010Brain, OAllan, PSimmons, AAutophagy is important in immune cells as a means of disposing of pathogens and in connecting with the antigen presentation machinery to facilitate immune priming and initiation of a correctly targeted adaptive immune response. While Toll-like receptors (TLRs) are known to regulate autophagy in this context, the extent to which other pattern recognition receptors (PRRs) are involved has been unclear. NOD2 is an intracellular PRR of the Nod-like receptor (NLR) family that is notable in that variants in the ligand recognition domain are associated with Crohn disease (CD). Our recent study shows NOD2 activates autophagy in a manner requiring ATG16L1, another CD susceptibility gene. NOD2 autophagy induction is required for bacterial handling and MHC class II antigen presentation in human dendritic cells (DCs). CD patients DCs expressing CD risk variant NOD2 or ATG16L1 display reduced autophagy induction after NOD2 triggering resulting in reduced bacterial killing and defective antigen presentation. Aberrant bacterial handling and immune priming could act as a trigger for inflammation in CD.
spellingShingle Brain, O
Allan, P
Simmons, A
NOD2-mediated autophagy and Crohn disease.
title NOD2-mediated autophagy and Crohn disease.
title_full NOD2-mediated autophagy and Crohn disease.
title_fullStr NOD2-mediated autophagy and Crohn disease.
title_full_unstemmed NOD2-mediated autophagy and Crohn disease.
title_short NOD2-mediated autophagy and Crohn disease.
title_sort nod2 mediated autophagy and crohn disease
work_keys_str_mv AT braino nod2mediatedautophagyandcrohndisease
AT allanp nod2mediatedautophagyandcrohndisease
AT simmonsa nod2mediatedautophagyandcrohndisease