NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection
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L. Kiemeney | S. Vermeulen | T. Plantinga | I. Mysorekar | Caihong Wang | Graziella R Mendonsa | Xuejun Yuan | E. Ma
[1] A. Amendola,et al. Nod2 deficiency is associated with an increased mucosal immunoregulatory response to commensal microorganisms , 2013, Mucosal Immunology.
[2] Vanessa M. Hubbard-Lucey,et al. A deficiency in the autophagy gene Atg16L1 enhances resistance to enteric bacterial infection. , 2013, Cell host & microbe.
[3] Paul G. Thomas,et al. Receptor interacting protein kinase 2-mediated mitophagy regulates inflammasome activation during virus infection , 2013, Nature Immunology.
[4] I. Mysorekar,et al. ATG16L1 and pathogenesis of urinary tract infections , 2012, Autophagy.
[5] Jong-Hwan Park,et al. Nucleotide-binding oligomerization domain 2 (Nod2) is dispensable for the innate immune responses of macrophages against Yersinia enterocolitica , 2012, Journal of Microbiology.
[6] Qunyuan Zhang,et al. Atg16L1 deficiency confers protection from uropathogenic Escherichia coli infection in vivo , 2012, Proceedings of the National Academy of Sciences.
[7] M. Bringer,et al. Defects in autophagy favour adherent‐invasive Escherichia coli persistence within macrophages leading to increased pro‐inflammatory response , 2012, Cellular microbiology.
[8] J. Hugot,et al. Yersinia pseudotuberculosis effector YopJ subverts the Nod2/RICK/TAK1 pathway and activates caspase-1 to induce intestinal barrier dysfunction. , 2012, Cell host & microbe.
[9] Fernanda S. Oliveira,et al. Nucleotide-Binding Oligomerization Domain-1 and -2 Play No Role in Controlling Brucella abortus Infection in Mice , 2011, Clinical & developmental immunology.
[10] L. Joosten,et al. ATG16L1 polymorphisms are associated with NOD2-induced hyperinflammation , 2011, Autophagy.
[11] N. Warner,et al. The Nod2 sensor promotes intestinal pathogen eradication via the chemokine CCL2-dependent recruitment of inflammatory monocytes. , 2011, Immunity.
[12] M. Oosting,et al. Crohn's disease-associated ATG16L1 polymorphism modulates pro-inflammatory cytokine responses selectively upon activation of NOD2 , 2011, Gut.
[13] Tariq Ahmad,et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci , 2010, Nature Genetics.
[14] C. Streutker,et al. Nod1 and Nod2 Regulation of Inflammation in the Salmonella Colitis Model , 2010, Infection and Immunity.
[15] A. Darfeuille‐Michaud,et al. Abnormalities in the Handling of Intracellular Bacteria in Crohn's Disease , 2010, Journal of clinical gastroenterology.
[16] R. Xavier,et al. Crohn's disease‐associated adherent‐invasive E. coli are selectively favoured by impaired autophagy to replicate intracellularly , 2010, Cellular microbiology.
[17] D. Philpott,et al. Role of Nod1 in Mucosal Dendritic Cells during Salmonella Pathogenicity Island 1-Independent Salmonella enterica Serovar Typhimurium Infection , 2009, Infection and Immunity.
[18] S. Hultgren,et al. A murine model of urinary tract infection , 2009, Nature Protocols.
[19] J. Mills,et al. Bone morphogenetic protein 4 signaling regulates epithelial renewal in the urinary tract in response to uropathogenic infection. , 2009, Cell host & microbe.
[20] Sarah L. Brown,et al. A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells , 2008, Nature.
[21] Tony Fletcher,et al. Sequence variant on 8q24 confers susceptibility to urinary bladder cancer , 2008, Nature Genetics.
[22] M. Daly,et al. Impaired Autophagy of an Intracellular Pathogen Induced by a Crohn's Disease Associated ATG16L1 Variant , 2008, PloS one.
[23] J. Hugot,et al. Nod2 Mediates Susceptibility to Yersinia pseudotuberculosis in Mice , 2008, PloS one.
[24] P. Humphrey,et al. Detection of Intracellular Bacterial Communities in Human Urinary Tract Infection , 2007, PLoS medicine.
[25] R. Xavier,et al. Unravelling the pathogenesis of inflammatory bowel disease , 2007, Nature.
[26] S. Fisher,et al. A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn's disease and is independent of CARD15 and IBD5. , 2007, Gastroenterology.
[27] Judy H Cho,et al. Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis , 2007, Nature Genetics.
[28] G. Núñez,et al. RICK/RIP2 Mediates Innate Immune Responses Induced through Nod1 and Nod2 but Not TLRs1 , 2007, The Journal of Immunology.
[29] D. Philpott,et al. Nod-like proteins in immunity, inflammation and disease , 2006, Nature Immunology.
[30] S. Hultgren,et al. Mechanisms of uropathogenic Escherichia coli persistence and eradication from the urinary tract , 2006, Proceedings of the National Academy of Sciences.
[31] Michael Karin,et al. Nod2 Mutation in Crohn's Disease Potentiates NF-κB Activity and IL-1ß Processing , 2005, Science.
[32] Richard A. Flavell,et al. Nod2-Dependent Regulation of Innate and Adaptive Immunity in the Intestinal Tract , 2005, Science.
[33] S. Hultgren,et al. Intracellular Bacterial Biofilm-Like Pods in Urinary Tract Infections , 2003, Science.
[34] Y. Ogura,et al. Genetic variation and activity of mouse Nod2, a susceptibility gene for Crohn's disease. , 2003, Genomics.
[35] M. Chamaillard,et al. Nod2 Is a General Sensor of Peptidoglycan through Muramyl Dipeptide (MDP) Detection* , 2003, The Journal of Biological Chemistry.
[36] S. Foster,et al. Host Recognition of Bacterial Muramyl Dipeptide Mediated through NOD2 , 2003, The Journal of Biological Chemistry.
[37] Judy H. Cho,et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease , 2001, Nature.
[38] Mourad Sahbatou,et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease , 2001, Nature.
[39] D. Jewell,et al. NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation , 2010, Nature Medicine.
[40] D. Philpott,et al. Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry , 2010, Nature Immunology.
[41] Judy H. Cho,et al. Crohn's disease-associated NOD2 variants share a signaling defect in response to lipopolysaccharide and peptidoglycan. , 2003, Gastroenterology.