Abstract
Crohn's disease is a chronic inflammatory bowel disorder that has been associated with polymorphisms in the genes encoding the pattern-recognition receptor NOD2 and the autophagic regulator ATG16L1. A new study demonstrates that NOD2 recruits ATG16L1 at bacterial entry sites, thereby bridging innate immunity and autophagy.
MeSH terms
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Animals
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Autophagy / genetics
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Autophagy / immunology*
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Autophagy / physiology
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Autophagy-Related Proteins
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Bacterial Infections / immunology*
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Bacterial Infections / physiopathology*
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Carrier Proteins / genetics
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Carrier Proteins / physiology
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Crohn Disease / genetics
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Crohn Disease / immunology
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Crohn Disease / physiopathology
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Humans
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Immunity, Innate* / genetics
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Immunity, Innate* / physiology
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Models, Biological
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Mutation
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Nod2 Signaling Adaptor Protein / genetics
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Nod2 Signaling Adaptor Protein / physiology
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Signal Transduction
Substances
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ATG16L1 protein, human
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Autophagy-Related Proteins
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Carrier Proteins
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NOD2 protein, human
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Nod2 Signaling Adaptor Protein