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Related Experiment Videos

DcR3/TR6 effectively prevents islet primary nonfunction after transplantation.

Yulian Wu1, Bing Han, Hongyu Luo

  • 1Laboratory of Transplantation Immunology, Centre hospitalier de l'Universite de Montreal, Montreal, Quebec, Canada.

Diabetes
|August 28, 2003
PubMed
Summary

Primary nonfunction (PNF) of transplanted islets, a major obstacle, can be prevented. The study shows that TR6, a decoy receptor, protects islets from Fas-mediated apoptosis, suggesting a novel strategy for clinical islet transplantation.

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Cell Death Pathways

Background:

  • Primary nonfunction (PNF) is a significant barrier to successful islet transplantation.
  • DcR3/TR6 is a soluble decoy receptor that inhibits apoptosis mediated by tumor necrosis factor (TNF) receptor family members.
  • Fas-mediated apoptosis is implicated in PNF.

Purpose of the Study:

  • To investigate the potential of TR6 in preventing PNF after islet transplantation.
  • To elucidate the role of Fas-mediated apoptosis in PNF.
  • To evaluate TR6 as a therapeutic strategy for PNF.

Main Methods:

  • Islet transplantation in syngeneic and allogeneic models.
  • In vitro treatment of islets with FasL and IFN-gamma, with and without TR6.

Related Experiment Videos

  • Assessment of apoptosis and insulin release.
  • In vivo experiments using Fas-deficient mice (lpr/lpr and gld/gld).

    • Main Results:

    • Untreated islet transplantation showed PNF rates of 25% (isogeneic) and 26.5% (allogeneic).
    • TR6 administration completely prevented PNF in allogeneic transplantation.
    • TR6 significantly reduced FasL and IFN-gamma-induced islet apoptosis and preserved insulin release.
    • Syngeneic islet transplantation in Fas-deficient mice was more effective than in wild-type mice.

    Conclusions:

    • Fas-mediated apoptosis plays a critical role in islet primary nonfunction.
    • TR6 effectively protects beta-cells from FasL and IFN-gamma-induced damage.
    • TR6 represents a promising novel therapeutic strategy to prevent PNF in clinical islet transplantation.