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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 goblet,...
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Updated: Jun 5, 2026

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
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Published on: January 25, 2017

MAIT Cells Maintain Intestinal Homeostasis Through IL-22 in an Experimental Colitis.

Yanan Peng1,2, Chunlan Zheng1,2, Youwei Wang1,2

  • 1Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, People's Republic of China.

Journal of Inflammation Research
|June 4, 2026
PubMed
Summary
This summary is machine-generated.

Mucosa-associated invariant T (MAIT) cells protect the gut barrier during colitis by coordinating IL-22 production. This involves a novel MAIT-CCL2-AHR-IL-22 pathway crucial for mucosal repair in inflammatory conditions.

Keywords:
CCL2IL-22MAIT cellacute experimental colitisinflammatory bowel diseaseintestinal barrier

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Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells
08:22

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

Published on: March 23, 2022

Area of Science:

  • Immunology
  • Gastroenterology

Background:

  • Mucosa-associated invariant T (MAIT) cells are abundant in the gut but their role in intestinal homeostasis is unclear.
  • Investigating MAIT cell function in epithelial barrier integrity during experimental colitis is crucial.

Purpose of the Study:

  • To elucidate the role of MAIT cells in maintaining epithelial barrier integrity during experimental colitis.
  • To identify the molecular mechanisms by which MAIT cells influence intestinal homeostasis.

Main Methods:

  • Dextran sulfate sodium (DSS)-induced colitis in wild-type (WT) and MR1-deficient (MR1-/-) mice.
  • Assessment of disease severity, barrier function (FITC-dextran permeability, tight junction proteins), and bacterial translocation.
  • Single-cell RNA sequencing (scRNA-seq) to identify MAIT-cell-associated mediators, followed by rescue experiments with IL-22 or CCL2.

Main Results:

  • MAIT cells accumulate and activate in inflamed colons during DSS colitis.
  • MR1-/- mice exhibit exacerbated colitis, impaired barrier function, and increased bacterial translocation.
  • MAIT cell deficiency reduces IL-22 production; IL-22 and CCL2 rescue partially ameliorate colitis and restore barrier integrity.

Conclusions:

  • A novel MAIT-CCL2-AHR-IL-22 regulatory axis contributes to epithelial barrier protection during colitis.
  • MAIT cells act as upstream coordinators of IL-22-dependent mucosal repair.
  • Targeting this pathway offers potential for treating intestinal inflammatory diseases.