Animal models of chronic allograft injury: contributions and limitations to understanding the mechanism of long-term graft dysfunction

Transplantation. 2010 Nov 15;90(9):935-44. doi: 10.1097/TP.0b013e3181efcfbc.

Abstract

Advances in immunosuppression have reduced the incidence of acute graft loss after transplantation, but long-term allograft survival is still hindered by the development of chronic allograft injury, a multifactorial process that involves both immunologic and nonimmunologic components. Because these components become defined in the clinical setting, development of animal models enables exploration into underlying mechanisms leading to long-term graft dysfunction. This review presents animal models that have enabled investigation into chronic allograft injury and discusses pivotal models currently being used. The mechanisms uncovered by these models will ultimately lead to development of new therapeutic options to prevent long-term graft dysfunction.

Publication types

  • Editorial
  • Review

MeSH terms

  • Age Factors
  • Animals
  • Aorta / transplantation
  • Chronic Disease
  • Female
  • Graft Rejection / immunology*
  • Graft Rejection / pathology
  • Heart Transplantation / adverse effects
  • Heart Transplantation / immunology
  • Heart Transplantation / pathology
  • Humans
  • Kidney Transplantation / adverse effects
  • Kidney Transplantation / immunology
  • Kidney Transplantation / pathology
  • Lung Transplantation / adverse effects
  • Lung Transplantation / immunology
  • Lung Transplantation / pathology
  • Male
  • Mice
  • Models, Animal
  • Rats
  • Rats, Inbred F344
  • Rats, Inbred Lew
  • Transplantation, Homologous / adverse effects*
  • Transplantation, Homologous / immunology
  • Transplantation, Homologous / pathology
  • Treatment Outcome