The immunological and genetic basis of inflammatory bowel disease

By G. Bouma, W. Strober. Nature reviews. Immunology, 2003

1,861 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d2618239cd28744a4a1352393449b4897fc4a5ab

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Citations in the corpus

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”
The key role of segmented filamentous bacteria in the coordinated maturation of gut helper T cell responses. (2009, background): “…immune system in ‘‘tolerating’’ the gut microbiota has been greatly re-enforced by the increasing evidence that defects in both immune response and microbial recognition genes are central to the onset of inflammatory bowel diseases in genetically predisposed individuals (Bouma and Strober, 2003).”
The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis (2010, positive): “In addition, studies in rodents have linked tissue damage and disruption of the epithelial barrier in the gut to cytokine imbalances (Bouma and Strober, 2003).”
The gut microbiome shapes intestinal immune responses during health and disease (2009, neutral): “The causes of these diseases are complex and include contributions from genetic, geographic and habitual factor”
Bacterial flagellin is a dominant antigen in Crohn disease. (2004, background): “Discussion Data from both humans and experimental animals underscore the critical role of intestinal bacteria in the establishment and maintenance of IBD (2).”
Human adult stem cells derived from adipose tissue protect against experimental colitis and sepsis (2009, background): “3 Recent evidence supports the notion that an imbalance between effector T cells and Treg, probably by a defect in the Treg repertory, results in expansion of self-reactive T cells and inflammation.(3) The failure in the current treatments for IBD illustrates the need for novel therapeutic approache”
Intestinal immune homeostasis is regulated by the crosstalk between epithelial cells and dendritic cells (2005, neutral): “We then tested whether the T H 1-mediated pathology in inflammatory bowel diseases such as Crohn diseas”
Cytokine regulation of tight junctions (2008, background): “Interferon gamma (IFN-γ) is a Th1 pro-inflammatory cytokine found at elevated levels in the intestinal mucosa of IBD patients [10-12].”
Generation of regulatory dendritic cells and CD4+Foxp3+ T cells by probiotics administration suppresses immune disorders (2010, background): “Decreased Tregs are associated with inflammatory diseases, including IBD and AD (29, 30).”
Mechanisms of Disease: Inflammatory Bowel Diseases. (2019, background): “In turn Th1 and Th17 cells secrete the pro-inflammatory cytokines IL-17, INF-γ and TNFa that feed into a self-sustaining amplification cycle whereby they stimulate APC, macrophages, fibroblasts and endothelial cells to produce TNFα, IL-1, IL-6, IL-8, IL-12 and IL-18 (5, 22, 98).”
The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, positive): “In addition, abnormal Th1 cell responses have been demonstrated to mediate, at least in part, many other autoimmune diseases, including psoriasis and inflammatory bowel disease (IBD) (Bouma and Strober, 2003; Lowes et al., 2007).”