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Related Concept Videos

Renewal of Intestinal Stem Cells01:23

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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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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.
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Inflammatory Bowel Disease II: Crohn's Disease01:30

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Introduction
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Crohn's disease
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Updated: Jul 12, 2025

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation.

Tzu-Yu Shao1, Tony T Jiang1, Joseph Stevens2

  • 1Division of Infectious Diseases, Center for Inflammation and Tolerance, University of Cincinnati School of Medicine, Cincinnati, OH 45229, USA.

Cell Reports
|October 27, 2023
PubMed
Summary

The Kruppel-like factor 2 (KLF2) regulates CD4 T cells crucial for immune tolerance to gut microbes. These KLF2+ CD4 cells prevent intestinal inflammation, a finding relevant to Crohn's disease.

Keywords:
CD4 T cellCP: ImmunologyCandida albicansCrohn's diseaseTr1 cellbacterial flagellin Cbir1commensal toleranceinflammatory bowel diseaseintestinal inflammationmicrobiota

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Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Commensal microbiota colonization requires robust peripheral immune tolerance.
  • CD4 T cells play a critical role in maintaining gut homeostasis and preventing inflammation.

Purpose of the Study:

  • To investigate the role of the transcriptional regulator Kruppel-like factor 2 (KLF2) in CD4 T cell function related to immune tolerance.
  • To determine the necessity of KLF2+ CD4 cells in preventing microbiota-driven intestinal inflammation.

Main Methods:

  • Analysis of KLF2 expression in CD4 T cells from lymphoid and intestinal tissues.
  • Generation of mice with conditional KLF2 deficiency in T cells.
  • Assessment of intestinal inflammation and rectal prolapse in KLF2-deficient mice.
  • In vitro and in vivo functional assays of KLF2+ CD4 cells and IL-10 production.
  • Evaluation of KLF2+ CD4 cell accumulation in Crohn's disease patients.

Main Results:

  • CD4 T cells specific for commensal microbes are enriched for KLF2 expression.
  • Conditional KLF2 deficiency in T cells leads to spontaneous intestinal inflammation and rectal prolapse.
  • These inflammatory phenotypes are reversed by microbiota elimination or reconstitution with KLF2+ cells.
  • Activated KLF2+ cells produce IL-10, which is essential for their suppressive function and protection against inflammation.
  • Reduced KLF2+ CD4 cell numbers are observed in Crohn's disease patients.

Conclusions:

  • KLF2 is essential for a specific subpopulation of CD4 T cells, identified as T regulatory type 1 (Tr1) cells, to maintain tolerance to commensal microbiota.
  • KLF2+ CD4 T cells, through IL-10 production, are critical for preventing intestinal inflammation.
  • Dysregulation of KLF2+ CD4 T cells may contribute to inflammatory conditions like Crohn's disease.