Inflammatory bowel disease and mutations affecting the interleukin-10 receptor.

By E. Glocker, D. Kotlarz, K. Boztug, E. Gertz, Alejandro A. Schäffer, F. Noyan, M. Perro, J. Diestelhorst, A. Allroth, Dhaarini Murugan and 18 more. New England Journal of Medicine, 2009

1,378 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/83ab1feb710fb48979cb703b053ec9bed3a9852b

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Citations in the corpus

Pediatric modification of the Montreal classification for inflammatory bowel disease: The Paris classification (2011, background): “The suspicion of a monogenetic cause of these early onset forms was recently confirmed by the discovery of mutations in the genes coding for one of the two IL10 receptors causing impaired IL10 signaling.(35) These findings indicate a new view of IBD as a continuum in physiopathogenic mechanisms from”
New IBD genetics: common pathways with other diseases (2011, background): “IBD-like phenotype in the first year of life.(33) Other noteworthy IBD susceptibility genes include IL1R2, REL, CARD9, NKX2.”
Intestinal homeostasis and its breakdown in inflammatory bowel disease (2011, background): “Evidence for the role of IL-10 in human IBD comes from findings that mutations in the IL-10 receptor genes IL10RA and IL10RB lead to severe early-onset IB”
Pathomechanisms of Oxidative Stress in Inflammatory Bowel Disease and Potential Antioxidant Therapies (2017, background): “Along with the IL-23R pathway, the susceptibility genes IL-12B, JAK2, and SATA3 have also been discovered in CD [98], whereas polymorphisms in IL-22 and IL-10 receptor 2 have been found, respectively, in UC patients and children with early-onset enterocolitis [79, 99].”
The immune system and the gut microbiota: friends or foes? (2010, background): “and in individuals with impaired intestinal immunoregulation, most notably in those who lack a functional IL-10 signalling pathwa”
GENETICS AND PATHOGENESIS OF INFLAMMATORY BOWEL DISEASE (2016, background): “These patients are characterized by refractory colitis and perianal disease but lack significant small intestinal involvement (26, 27).”
The Microbiome in Infectious Disease and Inflammation (2012, neutral): “Indeed, many reports have shown that the microbial populations in the intestine of IBD patients are different from those of healthy individuals (12–14).”
Current understanding of dysbiosis in disease in human and animal models (2016, background): “increased proinflammatory cytokines, most notably an increase in tumor necrosis factor a, from peripheral blood mononuclear cells.(81,84) The lack of an anti-inflammatory response and the subsequent increase in proinflammatory cytokines is especially severe in the intestine, where the presence of co”
Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. (2019, background): “Notably, MNPs from mice and patients with defective IL- 10R signalling produce colitogenic amounts of IL-1β, highlighting the importance of intact IL10 signalling in MNPs to suppress inflammation (Shouval et al., 2016).”