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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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Inflammatory Bowel Disease I: Ulcerative Colitis

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Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
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Inflammatory bowel disease (IBD) encompasses two major chronic disorders—ulcerative colitis and Crohn’s disease—each characterized by relapsing episodes of gastrointestinal inflammation. Although they share certain clinical features, their patterns of involvement and manifestations differ in ways that aid diagnosis and guide management.Ulcerative ColitisUlcerative colitis is limited to the colon and rectum and involves continuous inflammation of the mucosal layer. The disease course is marked...
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Related Experiment Video

Updated: Jul 10, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Selective decrease in colonic CD56(+) T and CD161(+) T cells in the inflamed mucosa of patients with ulcerative

Masaru Shimamoto1, Yoshitaka Ueno, Shinji Tanaka

  • 1Department of Medicine and Molecular Science, Hiroshima University, Hiroshima 734-8551, Japan.

World Journal of Gastroenterology
|November 21, 2007
PubMed
Summary

A reduction in colonic mucosal NK receptor-positive T (NKR(+) T) cells may contribute to ulcerative colitis (UC) inflammation. These specific T cells, including CD56(+) and CD161(+) subsets, were significantly decreased in inflamed UC tissues.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
  • The role of specific immune cells in the colonic mucosa of UC patients requires further elucidation.
  • Natural Killer Receptor-positive T (NKR(+) T) cells are present in the human colon.

Purpose of the Study:

  • To investigate the role of colonic mucosal NK receptor-positive T (NKR(+) T) cells in regulating intestinal inflammation.
  • To analyze the population and function of NKR(+) T cells in ulcerative colitis (UC).

Main Methods:

  • Colonic mucosal tissues from 96 UC patients and 18 controls were analyzed using flow cytometry.
  • NK receptor-positive T cell subsets (CD56(+) and CD161(+)) were quantified.
  • Intracellular interleukin-10 (IL-10) expression in NKR(+) T cells was assessed after in vitro stimulation.

Main Results:

  • Populations of CD56(+) T cells and CD161(+) T cells were significantly reduced in inflamed UC mucosa compared to controls.
  • The frequency of NKR(+) T cells inversely correlated with UC inflammation severity (Matts' classification).
  • Approximately 4% of mucosal NKR(+) T cells expressed the anti-inflammatory cytokine IL-10.

Conclusions:

  • A selective reduction in colonic mucosal NKR(+) T cells may contribute to the pathogenesis of intestinal inflammation in UC.
  • These findings highlight a potential role for NKR(+) T cells in maintaining intestinal homeostasis.