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Accelerated graft arteriosclerosis is enhanced by sensitization of the recipient to donor lymphocytes.

The development of arteriosclerosis is the most serious and common complication in long-term survivors of cardiac transplantation.1 We recently have demonstrated that heart grafts exchanged between inbred rat strains with selected histocompatibility differences develop accelerated graft arteriosclerosis.2 Heterotopic cardiac allografts were exchanged between strains that differed for MHC class 1 (RT1.A or RT1.E) antigens or groups of minor, non-MHC antigens in MHC-compatible congenic combinations. In combinations in which the allograft reaction is mild and prolonged, the donor hearts exhibit pathological changes that include a diffuse, interstitial myocardial fibrosis, perivascular fibrosis, and intimal proliferation in arteries of the graft myocardium. The results suggested that the comparable pathological changes seen in long-term human cardiac survivors may reflect low-level, persistent allograft reactions rather than factors associated with graft anoxia or effects of immunotherapy to prevent graft rejection. 
 
The observation that accelerated graft arteriosclerosis could be induced as the result of low-level, persistent allograft reactions suggests that manipulations of this allograft reaction should be associated with alterations in the severity or prevalence of the lesions in the heart graft. In the studies reported here, we have extended these early observations to examine the influence of immunization of recipient animals with donor tissues on the pathological lesions in the donor heart.