The genetics and immunopathogenesis of inflammatory bowel disease

By Judy H. Cho. Nature reviews. Immunology, 2008

990 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c28478d06e7cc98560c9252e714d4c253eb34f89

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

In Immunology

Citations in the corpus

Potential etiologic and functional implications of genome-wide association loci for human diseases and traits (2009, background): “Although some of these aspects have been examined on a smaller scale for individual diseases such as type 2 diabetes (2), inflammatory bowel disease (3), and cancer (4), a comprehensive genome-wide analysis across all GWAS pub lished to date has not been conducted.”
Scalable Variational Inference for Bayesian Variable Selection in Regression, and Its Accuracy in Genetic Association Studies (2012, background): “Although the variants identified so far account for only a portion of the variance in disease risk, many of these variants are believed to play an important biological role in signaling pathways that regulate responses to pathogens (Cho 2008).”
Pattern recognition receptors and inflammation. (2010, background): “A mutation in NOD2 that generates a truncated form of the protein is frequently found in patients with Crohn’s disease, an inflammatory bowel disorder (Cho, 2008).”
Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells. (2012, background): “Failure to maintain this exquisite balance and hyperresponsiveness in genetically predisposed individuals results in chronic inflammatory bowel disorders (IBD) such as Crohn’s disease and ulcerative colitis (Cho, 2008).”
Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*). (2009, background): “CD and ulcerative colitis (UC) are the two most common forms of inflammatory bowel disease (IBD), but there are several clinical as well as genetic features that distinguish between them (163).”
Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility (2011, background): “SNPs in or near CARD9 and PTGER4 (encoding prostaglandin E receptor 4, EP4 subtype) have also been associated with Crohn's disease previousl”
Nod2 is required for the regulation of commensal microbiota in the intestine (2009, background): “Although the exact mechanism by which Nod2 mutations contribute to Crohn’s disease pathogenesis is still unclear, loss-offunction mutations in Nod2 have been suggested to alter host microbial interactions through various mechanisms, including altered antimicrobial activity of Paneth cells in the ter”
Genes and Molecules of Lactobacilli Supporting Probiotic Action (2008, background): “This is particularly of interest for IBD, as a genetic link between NOD2 mutations and susceptibility to Crohn’s disease exists, mainly in European and North American patients (48).”
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): “The current generally accepted disease hypothesis is that the chronic inflammation of IBD results from a genetically dysregulated host immune response directed at the gut microbiota [6-8].”
STAT3 signaling in immunity (2016, background): “, single nucleotide polymorphisms, SNPs) with increased predisposition to psoriasis and multiple sclerosis; STAT3 SNPs are also linked with inflammatory bowel disease [73–76].”