GRAFT ADAPTATION

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Abstract
Long-term surviving (100 to 120 days) renal allografts were retransplanted to fresh recipients syngeneic with the original host in three donor-recipient combinations: DA to LEW, (DA × LEW)F1 to LEW, and (DA × LEW)F1 to DA. The results were markedly different in the three combinations. Long-term surviving grafts in the DA to LEW model were rejected as vigorously as fresh grafts, while in the F1 to DA model they survived indefinitely without any impairment of graft function at any stage. In the F1 to LEW models most grafts underwent acute rejection, but the majority recovered to survive for prolonged periods with impaired graft function. It was found that long-term surviving grafts in the DA to LEW and F1 to LEW models were almost completely unable to induce lymphocytotoxin responses, in marked contrast to the strong responses seen with the use of fresh kidney grafts. The mechanism of graft adaptation was examined in three ways. First, quantitative absorption analysis on each of six long-term surviving DA and four long-term surviving F1 kidneys from LEW hosts showed that the amount of incompatible RT-1B (Ia) antigens was normal, whereas the amount of incompatible RT-1A (SD) antigen was, surprisingly, increased by a factor of 3. These results excluded antigen modulation and antigen masking as the mechanism of adaptation. Second, the possibility that graft endothelium is replaced by host endothelium was excluded by showing that long-term surviving DA kidney grafts could be hyperacutely rejected by injecting alloantisera and complement. Finally, attempts to replace passenger leukocytes by injecting donor blood at the time of grafting were not successful.