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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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

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...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

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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Related Experiment Video

Updated: May 16, 2026

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
06:57

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Published on: September 18, 2016

IL-23 in colitis: targeting the progenitors.

Ce Tang1, Yoichiro Iwakura

  • 1Research Institute for Biomedical Sciences, Tokyo University of Science, Yamazaki 2669, Noda-shi, Chiba, Japan.

Immunity
|December 19, 2012
PubMed
Summary

Interleukin-23 (IL-23) dysregulates hematopoietic stem and progenitor cells, contributing to inflammatory bowel disease (IBD) development. This finding offers new insights into IBD pathogenesis and potential therapeutic targets.

Area of Science:

  • Immunology
  • Gastroenterology
  • Stem Cell Biology

Background:

  • Inflammatory bowel disease (IBD) encompasses chronic gastrointestinal inflammation.
  • Understanding the cellular and molecular drivers of IBD pathogenesis is crucial for developing effective treatments.

Discussion:

  • Griseri et al. demonstrate that Interleukin-23 (IL-23) signaling disrupts the normal function of hematopoietic stem and progenitor cells (HSPCs).
  • This dysregulation of HSPCs by IL-23 is shown to be a key factor in the development of experimental models of IBD.
  • The study highlights a novel mechanism linking innate immune signaling to stem cell dysfunction in the context of chronic gut inflammation.

Key Insights:

  • IL-23 plays a significant role in modulating HSPC behavior.
  • Aberrant HSPC function driven by IL-23 contributes directly to IBD pathology.

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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

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Last Updated: May 16, 2026

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
06:57

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Published on: September 18, 2016

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
10:30

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

  • This research identifies a critical link between immune mediators and stem cell populations in inflammatory diseases.
  • Outlook:

    • Further investigation into IL-23-HSPC interactions may reveal new therapeutic strategies for IBD.
    • Targeting the IL-23 pathway could offer a novel approach to managing IBD by restoring stem cell homeostasis.
    • This work opens avenues for exploring stem cell-based therapies in conjunction with immune modulation for IBD treatment.