The understanding of chronic rejection has been greatly enhanced by th
e 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 perpetua
tion of an ischemic state. Lesions of vasculopathy and parenchymal cel
l damage may proceed at different rates, but the vasculopathy seems re
versible until healing occurs. The experimental models that have led u
s to significant understanding are described herein.