Apoptosis of pancreatic beta-cells detected in accelerated diabetes of NOD mice: no role of Fas-Fas ligand interaction in autoimmune diabetes

Eur J Immunol. 1999 Feb;29(2):455-65. doi: 10.1002/(SICI)1521-4141(199902)29:02<455::AID-IMMU455>3.0.CO;2-A.

Abstract

Autoreactive T lymphocytes probably cause pancreatic beta-cell death by inducing apoptosis. To visualize apoptotic beta-cells in vivo, we accelerated diabetes of NOD mice with cyclophosphamide (CY) or adoptive transfer. We also studied whether Fas-mediated apoptosis is involved in the development of diabetes by administrating anti-Fas ligand (FasL) Ab and by grafting Fas-deficient neonatal pancreas from NOD-lpr/lpr mice. Apoptotic cells were clearly shown 8 days after CY treatment. Beta-cell apoptosis was also observed after adoptive transfer but in a different kinetic pattern. Anti-FasL Ab administration failed to inhibit diabetes after CY treatment or adoptive transfer, while it inhibited Con A-induced hepatitis. Fas-deficient neonatal pancreata were destroyed by lymphocytic infiltration in diabetic NOD mice. Our results clearly demonstrate apoptosis of beta-cells in accelerated diabetes and indicate that Fas-FasL interaction is not involved in diabetes of NOD mice, contrary to the previous reports.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Autoimmunity
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 1 / pathology*
  • Fas Ligand Protein
  • Islets of Langerhans / immunology
  • Islets of Langerhans / pathology*
  • Membrane Glycoproteins / immunology*
  • Mice
  • Mice, Inbred NOD
  • fas Receptor / immunology*

Substances

  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • fas Receptor