TGF-beta, T-cell tolerance and anti-CD3 therapy

Trends Mol Med. 2004 Jan;10(1):3-9. doi: 10.1016/j.molmed.2003.11.007.

Abstract

Recent studies by Chatenoud and co-workers suggest that non-mitogenic F(ab′)2 fragments of anti-CD3 antibodies, which cannot bind the Fc receptor, induce a prolonged period of tolerance and prevent diabetes in nonobese diabetic (NOD) mice. Tolerance is established by regulatory T cells through the production of transforming growth factor-β1 (TGF-β1), but the mechanism by which TGF-β1 confers this activity is unclear. Analysis of mice deficient in TGF-β1 suggests that TGF-β1 raises the threshold at which intracellular calcium activates T cells to a level that prevents an autoimmune response.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibodies / therapeutic use
  • Autoimmune Diseases / therapy*
  • CD3 Complex / immunology*
  • Calcium / pharmacology
  • Humans
  • Hypersensitivity, Immediate / prevention & control
  • Immune Tolerance*
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred NOD
  • T-Lymphocytes / immunology*
  • Transforming Growth Factor beta / physiology*
  • Transforming Growth Factor beta1

Substances

  • Antibodies
  • CD3 Complex
  • TGFB1 protein, human
  • Tgfb1 protein, mouse
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Calcium