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Updated: Aug 12, 2026

Isolating Lymphocytes from the Mouse Small Intestinal Immune System
11:28

Isolating Lymphocytes from the Mouse Small Intestinal Immune System

Published on: February 28, 2018

Regulation of cell death and survival in intestinal intraepithelial lymphocytes

T Brunner1, D Arnold, C Wasem

  • 1Division of Immunopathology, Institute of Pathology, University of Bern, Murtenstrasse 31, 3010 Bern, Switzerland. tbrunner@pathology.unibe.ch

Cell Death and Differentiation
|July 21, 2001
PubMed

Insights

Intraepithelial lymphocytes (IEL) in the gut undergo apoptosis upon isolation. Glucocorticoids contribute to this cell death, but T cell receptor activation can enhance IEL survival.

Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Intraepithelial lymphocytes (IEL) are crucial immune cells in the small intestine.
  • IEL reside within the intestinal epithelial layer, interacting closely with epithelial cells.
  • Isolation of IEL leads to significant apoptosis, indicating a dependence on their in vivo environment.

Purpose of the Study:

  • To investigate the mechanisms underlying IEL apoptosis upon ex vivo culture.
  • To determine the role of endogenous glucocorticoids in IEL cell death.
  • To explore the impact of T cell activation on IEL survival.

Main Methods:

  • Adrenalectomy and glucocorticoid receptor antagonist treatment in mice.
  • Ex vivo culture of isolated murine IEL.
  • Analysis of IEL apoptosis and survival.
  • Assessment of T cell receptor (TCR) activation effects on IEL.

Main Results:

  • Adrenalectomy and glucocorticoid receptor antagonist treatment significantly enhanced ex vivo IEL survival.
  • Ex vivo activation of IEL led to upregulation of anti-apoptotic genes.
  • TCR activation compensated for the lack of survival cytokines, rescuing IEL from apoptosis.

Conclusions:

  • Endogenously produced glucocorticoids contribute to IEL apoptosis.
  • TCR activation can counteract glucocorticoid-induced cell death in IEL.
  • IEL survival is regulated by the interplay between TCR activation and glucocorticoid signaling.

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