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Related Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

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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 II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

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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...
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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...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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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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Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

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Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
Diagnostic studies
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Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

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Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows...
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Related Experiment Video

Updated: Apr 21, 2026

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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DAB2IP modulates intestinal inflammation by enhancing ILC3 function in the gut.

Liang Liu1,2, Benjamin Davidorf1,2, Peixian Dong1,2

  • 1Department of Immunology and Immune Therapeutics, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.

Journal of Immunology (Baltimore, Md. : 1950)
|April 19, 2026
PubMed
Summary

DAB2IP regulates Group 3 innate lymphoid cells (ILC3s) to maintain intestinal barrier function. Loss of DAB2IP impairs cytokine production, compromising gut immunity and repair during inflammation.

Keywords:
DAB2IPcytokine productioninnate immunityinnate lymphoid cells 3 (ILC3)mucosal immunity

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Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells
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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Group 3 innate lymphoid cells (ILC3s) are crucial for intestinal barrier integrity, producing IL-22 and IL-17A.
  • The molecular mechanisms sustaining ILC3 cytokine production during inflammation are not fully understood.

Purpose of the Study:

  • To identify novel regulators of ILC3 effector function.
  • To elucidate the role of DAB2IP in maintaining mucosal immunity and epithelial repair.

Main Methods:

  • Analysis of human inflammatory bowel disease (IBD) mucosa.
  • Murine models of intestinal infection (Citrobacter rodentium) and colitis (DSS).
  • Genetic manipulation of DAB2IP in ILC3s.
  • Investigation of NF-κB signaling pathways.

Main Results:

  • Reduced DAB2IP expression in human IBD is linked to impaired epithelial repair.
  • Loss of DAB2IP in mice diminishes IL-22 and IL-17A production by ILC3s.
  • DAB2IP deficiency exacerbates intestinal inflammation and compromises host defense.
  • DAB2IP promotes ILC3 function by enhancing NF-κB activation and subsequent cytokine transcription.

Conclusions:

  • DAB2IP acts as a cell-intrinsic regulator of ILC3 effector function.
  • DAB2IP plays a critical role in mucosal immunity and epithelial repair.
  • Restoring DAB2IP signaling may offer a therapeutic strategy for intestinal inflammation.