SPARQL | HTML5 RDFa and Microdata document
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Ulcerative colitis signaling
http://purl.org/dc/terms/description
Ulcerative colitis (UC) together with Crohn’s disease (CD) are both chronic inflammation disorders in the gastrointestinal (GI) tract, and subtypes of inflammatory bowel disease (IBD). This inflammatory response in the GI tract is a result of various environmental and genetic components, microorganisms, and an impaired immune system. Among those many factors, changes in the luminal environment of the colonic epithelial cells are crucial and remain to be precisely analyzed. This pathway only considered UC, in which certain pathogens are found in increased or decreased amounts, compared to healthy controls.
In the upper section of the pathway, it is shown that the toll-like receptors (TLRs) recognized the components derived from microbes, such as flagellin, peptidoglycan (PGN), and lipopolysaccharide. As depicted on the left, also nucleotide-binding oligomerization domain (NOD) proteins, and antigen-presenting cells (APCs) recognized those microbial molecules. Activation of the TLR signaling pathway drives the upregulation of NF-kappa-B and its corresponding inflammation reaction. At the same time, the APC regulates the shift of naïve T-cells into effector T-cells and (Th2) and natural killer (NKT) T-cells. UC is mainly dominated by the Th2-type inflammation and the corresponding production of IL-4, IL-5, IL-13 and IL-10.
http://purl.org/dc/terms/identifier http://purl.org/dc/terms/references
https://identifiers.org/pubmed/23303670
http://purl.org/spar/cito/cites
https://identifiers.org/pubmed/32015337
https://identifiers.org/pubmed/17941072
https://identifiers.org/pubmed/26900284
https://identifiers.org/pubmed/25112700
https://identifiers.org/pubmed/23303670