Dependence of epithelial growth of the small intestine on T-cell activation during weaning in the rat

Gastroenterology. 1996 Jul;111(1):37-44. doi: 10.1053/gast.1996.v111.pm8698223.


Background & aims: Intestinal crypt hyperplasia is associated with local T-cell activation in both clinical and experimental examples of immunologically mediated enteropathy. This suggests that T cell-derived factors may be trophic for epithelial proliferation in the intestine postnatally. The purpose of this study was to investigate T-cell activity during weaning in the rat and to investigate immune dependence of intestinal growth on T-cell activation.

Methods: The expression of interleukin-2 receptor (IL-2R) by mesenteric lymph node T cells was investigated from days 14 to 160 of life. Rats were treated with monoclonal antibodies against the IL-2R that were nonblocking (control) or blocking (experimental) from day 7, and intestinal growth was assessed at days 19, 25, and 29 of life.

Results: The mean +/- SEM of T cells expressing the IL-2R during weaning (days 15-28) was 6.1% +/- 0.3% compared with 3.3% +/- 0.3% at other ages (P < 0.001). The small intestine in rats treated with blocking antibody had reduced crypt length and mitotic count compared with control animals.

Conclusions: Weaning is associated with activation of T cells and blockade of the IL-2R reduces intestinal growth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology
  • Dermatitis, Contact / immunology
  • Epithelium / growth & development
  • Epithelium / immunology
  • Female
  • Flow Cytometry
  • Intestinal Mucosa / growth & development
  • Intestinal Mucosa / immunology
  • Intestine, Small / growth & development*
  • Intestine, Small / immunology
  • Linear Models
  • Lymphocyte Activation*
  • Male
  • Rats
  • Rats, Inbred Strains
  • Receptors, Interleukin-2 / immunology
  • Receptors, Interleukin-2 / metabolism
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / physiology*
  • Weaning*


  • Antibodies, Monoclonal
  • Receptors, Interleukin-2