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Related Experiment Video

Updated: Jul 23, 2026

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade
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FasL-transfected endothelial cells decrease the proliferative response of allogeneic PBL.

Sandrine Cappellesso1, Gilles Thibault, Cyrille Hoarau

  • 1UPRES-EA 3249 Cellules Hématopoïétiques, Hémostase et Greffe, Faculté de Médecine, 2 bis boulevard Tonnelĺe 37032 Tours, France.

Transplant Immunology
|January 1, 2003
PubMed
Summary

Engineered endothelial cells expressing Fas ligand (FasL) can induce apoptosis in alloreactive T cells. This approach offers a potential strategy to reduce T cell proliferation and enhance graft survival in organ transplantation.

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In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

Published on: August 12, 2017

Area of Science:

  • Immunology
  • Transplantation Biology
  • Cell Biology

Background:

  • Graft endothelium critically regulates immune cell infiltration in organ transplantation.
  • Current immunosuppressive therapies for transplantation have limitations.
  • Immune-privileged sites utilize Fas ligand (FasL) to induce T cell apoptosis.

Purpose of the Study:

  • To investigate the potential of engineering endothelial cells to express FasL for inducing apoptosis in alloreactive T cells.
  • To evaluate the efficacy of FasL-expressing endothelial cells in inhibiting T cell proliferation in a transplantation context.

Main Methods:

  • Construction of an expression vector with human FasL cDNA.
  • Transfection of an endothelial cell line (ECV304) with the FasL vector.
  • Assessment of apoptosis induction in Jurkat T cells using FasL-transfected ECV304 cells.
  • Evaluation of alloreactive T cell proliferation inhibition in a mixed lymphocyte-endothelial cell co-culture model.

Main Results:

  • FasL-transfected ECV304 cells successfully induced apoptosis in Jurkat T cells, comparable to an anti-Fas antibody.
  • FasL-expressing ECV304 cells, while maintaining costimulatory pathways, inhibited alloreactive T cell proliferation.
  • Activated T cells underwent apoptosis when co-cultured with FasL-transfected ECV304 cells.

Conclusions:

  • Endothelial cells engineered to express FasL can effectively induce apoptosis in alloreactive T cells.
  • This strategy holds promise for inducing hyporesponsiveness of alloreactive T cells in organ transplantation.
  • FasL-expressing endothelial cells represent a potential novel therapeutic approach for improving graft survival.