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Nod2-mediated recognition of the microbiota is critical for mucosal adjuvant activity of cholera toxin

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Inflammatory Bowel Disease Genetics: Nod2

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Gut microbial DL-endopeptidase alleviates Crohn’s disease via the NOD2 pathway

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An Enterococcus faecium Secreted Antigen, SagA, Exhibits Broad-Spectrum Binding to Extracellular Matrix Proteins and Appears Essential for E. faecium Growth

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The antibacterial activity of sodium hypochlorite and chlorhexidine against Enterococcus faecalis: A review on agar diffusion and direct contact methods

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Intestinal macrophages arising from CCR2+ monocytes control pathogen infection by activating innate lymphoid cells

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REG gene expression in inflamed and healthy colon mucosa explored by in situ hybridisation

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Autophagy proteins suppress protective type I interferon signalling in response to the murine gut microbiota

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Decreased Paneth cell defensin expression in ileal Crohn's disease is independent of inflammation, but linked to the NOD2 1007fs genotype.

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NOD2 Expression in Intestinal Epithelial Cells Protects Toward the Development of Inflammation and Associated Carcinogenesis

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Enteric viruses evoke broad host immune responses resembling those elicited by the bacterial microbiome

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Cutting Edge: Crohn’s Disease-Associated Nod2 Mutation Limits Production of Proinflammatory Cytokines To Protect the Host from Enterococcus faecalis -Induced Lethality

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Interleukin-1β secretion induced by mucosa-associated gut commensal bacteria promotes intestinal barrier repair

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Hes1 promotes the IL-22-mediated antimicrobial response by enhancing STAT3-dependent transcription in human intestinal epithelial cells

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Reg4 and complement factor D prevent the overgrowth of E. coli in the mouse gut

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Peptidoglycan Metabolite Photoaffinity Reporters Reveal Direct Binding to Intracellular Pattern Recognition Receptors and Arf GTPases

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Role of regenerating islet-derived proteins in inflammatory bowel disease

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Resilience of the intestinal microbiota following pathogenic bacterial infection is independent of innate immunity mediated by NOD1 or NOD2

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Evaluation of Antibacterial Properties of Organic Gutta-percha Solvents and Synthetic Solvents Against Enterococcus faecalis

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Absence of NOD2 receptor predisposes to intestinal inflammation by a deregulation in the immune response in hosts that are unable to control gut dysbiosis

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There was collusion: Microbes in inflammatory bowel disease

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Reg4 protects against Salmonella infection-associated intestinal inflammation via adopting a calcium-dependent lectin-like domain

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B Cell Defects Observed in Nod2 Knockout Mice Are a Consequence of a Dock2 Mutation Frequently Found in Inbred Strains

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