The fundamental basis of inflammatory bowel disease.

By W. Strober, I. Fuss, P. Mannon. Journal of Clinical Investigation, 2007

1,354 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c649d7103dc600f8830c2cc9b13a2013902a2117

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In Epidemiology

1. M. Karin
2. R. Blumberg
3. Ramnik J. Xavier
4. S. Grivennikov
5. Markus F. Neurath

In Genetics

1. M. Karin
2. Q. Guan
3. D. Kufe
4. Wenjun Ouyang
5. Yan Zheng
6. Markus F. Neurath
7. H. Wexler
8. S. Shalapour

In Molecular Biology

1. S. Grivennikov
2. Sivakumar Vallabhapurapu
3. M. Karin
4. Q. Guan
5. D. Kufe
6. Ramnik J. Xavier
7. Markus F. Neurath
8. H. Wexler

Citations in the corpus

• STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing (2009, background): “…DEFINITIVE REPORT Inflammatory bowel diseases (IBDs) like Crohn’s disease and ulcerative colitis are thought to result from a dysregulated response of the intestinal immune system to bacteria present in the commensal flora (Strober et al., 2007; Rescigno, 2008).”
• Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. (2007, neutral): “The pathophysiology of IBD has been attributed to mucosal immune system dysregulation or gut microbiota and/or abnormal epithelial barrier function to (Strober et al., 2007).”
• A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “The resulting infiltration of the bowel by granulocytes and macrophages leads to a release of enzymes, reactive oxygen intermediates, and proinflammatory cytokines, all of which cause discontinuous ulceration and full thickness bowel wall inflammation often including granulomas [153, 154].”
• Specific microbiota direct the differentiation of Th17 cells in the mucosa of the small intestine (2008, neutral): “…of the microbiota has been suggested to influence susceptibility to inflammatory bowel diseases (IBD) (Elson et al., 2005; Sartor, 2008), which are mediated by both innate and adaptive arms of the host immune system (Coombes et al., 2005; Rakoff-Nahoum et al., 2004; Strober et al., 2007).”
• Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis (2011, neutral): “EM and tissue culture experiments were performed with endoscopic biopsy specimens collected in the endoscopy ward of the Department of Medicine 1.”
• Inflammatory responses and inflammation-associated diseases in organs (2015, background): “For example, CD is associated with excessive IFN-γ/IL-17 and IL-12/IL-23 production, while UC is associated with excess IL-13 [153].”
• Mucins in cancer: function, prognosis and therapy (2009, background): “IBD is thought to result from deregulated responses of the immune system to bacteria in the commensal flor”
• IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis. (2008, background): “In contrast, IL-23/IL-17 pathways have recently been shown to play a pathogenic role in experimental CD-like diseases (15, 16, 47, 48).”
• IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “IL-6 is also critical for T cell survival and differentiation and therefore has a central pathogenic role in T cell-dependent autoimmune disorders, including IBD (Atreya et al., 2000; Strober et al., 2007 ).”