NDT Advance Access originally published online on August 25, 2006
Nephrology Dialysis Transplantation 2006 21(11):3082-3086; doi:10.1093/ndt/gfl451
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The Fischer–Lewis model of chronic allograft rejection—a summary
Renal Transplant Unit, Glasgow Western Infirmary, Glasgow, Scotland, UK
Correspondence and offprint requests to: Maria L. Marco, Renal Transplant Unit, Glasgow Western Infirmary, Dumbarton Road, Glasgow G11 GNT, Scotland, UK. Email: mlmarco2003{at}yahoo.co.uk
Although the mechanisms involved in human allograft rejection differ in degree from those in animal allograft rejection, animal models are invaluable for the investigation of their cause and effect. A significant advantage of the animal model is that lesions, comparable with those seen in human allograft rejection, can be generated over a much shorter time scale. Chronic rejection in animal models seems to be driven principally by immune mechanisms, whereas a myriad of non-immune mechanisms are operating in human allograft rejection. Despite these limitations, well-established animal models allow investigators to manipulate allograft rejection and thereby make contributions to the understanding of its pathogenesis.
In addition, animal models provide the opportunity of identifying mechanisms whereby the rejection process might be arrested or reversed. Furthermore, such models have the potential of investigating the induction of tolerance by means that may be applicable to the human situation.
Chronic rejection has been studied using well-established and reproducible kidney allograft models in rats. In such models the histopathological changes observed in the rejecting renal allograft are similar to those occurring during chronic rejection in humans, and they provide a means of studying the underlying mechanisms involved in its pathogenesis.
Keywords: animal models of rejection; chronic allograft nephropathy; Fischer–Lewis model