Unravelling the pathogenesis of inflammatory bowel disease

By Ramnik J. Xavier, D. Podolsky. Nature, 2007

4,383 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/0e72ebb7b90b65086a10696ebc2e865ad6a855d6

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In Genetics

1. T. Kanai
2. K. Matsuoka
3. S. Brand
4. Judy H. Cho
5. L. Peyrin-Biroulet
6. J. Colombel
7. Andre Franke
8. Aviv Regev

In Immunology

1. T. Kanai
2. K. Matsuoka
3. C. Varol
4. Steffen Jung
5. S. Brand
6. B. B. Finlay
7. Aviv Regev
8. F. Powrie

Citations in the corpus

• Mechanisms of Disease: Inflammatory Bowel Diseases. (2019, background): “Acknowledgments: KA Papadakis is supported by Grant R03AI131011-01A1 from NIAID Abbreviations APC Antigen presenting cells CAMs Cellular adhesion molecules CD Crohn’s Disease GWAS Genome-wide association studies IBD Inflammatory Bowel Diseases IEC intestinal epithelial cells JAK Janus kinases Mayo C”
• Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47 (2011, background): “Though the precise etiology is unknown, the current hypothesis is a dysregulated mucosal immune response to commensal gut flora in genetically susceptible individual”
• Intestinal Goblet Cells and Mucins in Health and Disease: Recent Insights and Progress (2010, neutral): “microbes and microbial products [45, 72].”
• Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism (2018, background): “, 2015), and these are accompanied by increased intestinal permeability and enhanced intestinal bacteria infiltration, which can induce immune responses and ultimately systemic inflammation (Xavier and Podolsky, 2007; Martin-Subero et al., 2015).”
• Mucins in cancer: function, prognosis and therapy (2009, background): “Ulcerative colitis is a major form of idiopathic inflammatory bowel disease (IBD) that is characterized by marked inflammation, superficial mucosal ulceration, infiltration of neutrophils and depletion of goblet cell mucin”
• Nod2 is required for the regulation of commensal microbiota in the intestine (2009, background): “Changes in this homeostasis may influence susceptibility to or the progression of chronic inflammatory conditions in the intestine such as Crohn’s disease (1, 2).”
• Aberrant Mucin Assembly in Mice Causes Endoplasmic Reticulum Stress and Spontaneous Inflammation Resembling Ulcerative Colitis (2008, background): “Defects in these components have been implicated in human IBD, although fundamental knowledge of underlying pathogenesis remains very poorly understood, with even the most well-established defect, CARD15 mutations, elucidating only a subset of white patients with ileal Crohn’s disease [9,10], and wi”
• High-throughput clone library analysis of the mucosa-associated microbiota reveals dysbiosis and differences between inflamed and non-inflamed regions of the intestine in inflammatory bowel disease (2011, background): “prevalence of IBD in recent years, suggesting that environmental factors are also involved [5].”