The pathophysiology of chronic rejection.
The understanding of chronic rejection has been greatly enhanced by the use of genetically controlled experimental models using inbred rats. Models that express all lesions encountered in human transplants are described. Findings of chronic rejection depend on genetic disparity, strength of the immunologic reaction, response to injury, and perpetuation of an ischemic state. Lesions of vasculopathy and parenchymal cell damage may proceed at different rates, but the vasculopathy seems reversible until healing occurs. The experimental models that have led us to significant understanding are described herein.
Guttmann
R D
RD
Centre for Clinical Immunobiology and Transplantation, McGill University, Montreal, Quebec, Canada.
Forbes
R D
RD
Zheng
S X
SX
D000818:Animals; D016572:Cyclosporine / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D016232:Endothelins / Q000502:physiology; D006084:Graft Rejection / Q000276:immunology / Q000503:physiopathology*; D016027:Heart Transplantation / Q000276:immunology; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000276:immunology; D051381:Rats; D011919:Rats, Inbred Strains; D013601:T-Lymphocytes / Q000276:immunology
D016232:Endothelins; D007166:Immunosuppressive Agents; D016572:Cyclosporine