Regulated and endothelial cell-specific expression of Fas ligand: an in vitro model for a strategy aiming at inhibiting xenograft rejection

Transplantation. 1998 Nov 15;66(9):1126-31. doi: 10.1097/00007890-199811150-00002.

Abstract

Background: Immunologically privileged sites have been shown to express Fas ligand (FasL) and may protect themselves by inducing apoptosis of infiltrating inflammatory cells. We asked whether the Fas/FasL interaction could be used to protect a xenograft from rejection. We proposed that endothelial cells that are resistant to Fas-mediated killing could be considered as a vehicle for expression of recombinant FasL.

Methods: Based on the tetracycline-regulated expression system, constructs were designed that allow endothelial cell-specific and regulated expression of FasL by placing the tetracycline-dependent transactivator under control of the murine intercellular adhesion molecule-2 promoter.

Results: Primary bovine endothelial cells transfected with FasL efficiently killed Fas-expressing cells in a regulated manner. Not only Fas-positive cell lines but also human peripheral blood lymphocytes underwent apoptosis upon exposure to FasL-transfected endothelial cells.

Conclusion: This in vitro model may provide tools for the generation of transgenic animals to be used as donors for vascularized xenograft transplantation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / cytology
  • Apoptosis
  • Cattle
  • Cell Death
  • Endothelium, Vascular / cytology*
  • Endothelium, Vascular / metabolism*
  • Fas Ligand Protein
  • Graft Rejection / prevention & control
  • Humans
  • Jurkat Cells / physiology
  • Leukocytes, Mononuclear / cytology
  • Membrane Glycoproteins / biosynthesis*
  • Models, Immunological

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins