Key result
MHC disparities induce acute heart graft rejection in mice despite some combinations functioning ~100 days.
Both MHC class I and class II disparities can independently induce acute rejection of vascularized heart allografts in mice, with outcomes depending on specific donor-recipient combinations.
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MHC class I/II mismatches trigger acute murine cardiac rejection with occasional long-term survival; hypothesis-generating for alloantigen effects, translation to humans remains untested.
We have examined the role of entire major histocompatibility complex (MHC) disparity, individual class II or class I alloantigens in the rejection of vascularized heart allografts. Our results demonstrate that entire MHC, as well as both class II and class I disparities, may induce acute heart graft rejection or severe and irreversible heart muscle destruction. However, in 1 of 2 combinations differing at class II and 1 of 5 differing at class I, hearts have shown a good function greater than 100 days postgrafting. Furthermore, each donor-recipient combination has demonstrated a unique pattern of heart allograft function as well as a degree of heart muscle damage. In conclusion, these data suggest that the rejection process depends upon multiple factors such as the immune-response-gene-regulated immunoresponsiveness of the recipient as well as the expression of alloantigens on heart grafts during the induction and effector phases of the immune response.
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Stepkowski et al. (1987) studied Vascularized heart allograft rejection. MHC disparity (entire MHC, class I, or class II alloantigens) vs. Different donor-recipient combinations was evaluated on Heart graft rejection or heart muscle destruction. Entire MHC, class I, and class II disparities induced acute heart graft rejection in mice, though some specific combinations maintained good function for >100 days.
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