The Crohn’s disease polymorphism, ATG16L1 T300A, alters the gut microbiota and enhances the local Th1/Th17 response

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Genetic risk, dysbiosis, and treatment stratification using host genome and gut microbiome in inflammatory bowel disease

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Exploring the genetic architecture of inflammatory bowel disease by whole-genome sequencing identifies association at ADCY7

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Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice

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Population-based metagenomics analysis reveals markers for gut microbiome composition and diversity

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Gene-microbiota interactions contribute to the pathogenesis of inflammatory bowel disease

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The Dynamics of the Human Infant Gut Microbiome in Development and in Progression toward Type 1 Diabetes

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Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations

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Bacterial Sensor Nod2 Prevents Inflammation of the Small Intestine by Restricting the Expansion of the Commensal Bacteroides vulgatus

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A Crohn’s disease variant in Atg16l1 enhances its degradation by caspase 3

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Atg16L1 T300A variant decreases selective autophagy resulting in altered cytokine signaling and decreased antibacterial defense

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Atg16l1 is Required for Autophagy in Intestinal Epithelial Cells and Protection of Mice From Salmonella Infection

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Phylogenetic Analysis of Dysbiosis in Ulcerative Colitis During Remission

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Commensal Bacteroides Species Induce Colitis in Host-Genotype-Specific Fashion in a Mouse Model of Inflammatory Bowel Disease

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Enterobacteriaceae Act in Concert with the Gut Microbiota to Induce Spontaneous and Maternally Transmitted Colitis

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ATG16L1 and NOD2 Interact in an Autophagy-Dependent Antibacterial Pathway Implicated in Crohn's Disease Pathogenesis

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Supervised classification of microbiota mitigates mislabeling errors

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Microbiota innate stimulation is a prerequisite for T cell spontaneous proliferation and induction of experimental colitis

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Transcriptional activity of the dominant gut mucosal microbiota in chronic inflammatory bowel disease patients

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A common role for Atg16L1, Atg5, and Atg7 in small intestinal Paneth cells and Crohn disease

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Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry

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NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation

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Microbial Influences in Inflammatory Bowel Diseases

(2008) R. Balfour Sartor   GASTROENTEROLOGY

Twin studies reveal specific imbalances in the mucosa-associated microbiota of patients with ileal Crohnʼs disease

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A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells

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Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production

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