These experiments will more completely elucidate the reason for long-term survival of partially H-2 incompatible B10.BR primarily vascularized cardiac allografts in B10.A mice. Four avenues will be pursued: 1. To determine whether the host anti-donor alloreactive cells have been partly depleted, by testing the capacity of lymphocytes from long-term recipients to reconstitute a specific allograft response in sublethally irradiated mice, and by determining the reaction of a second naive host parabiosed to the heart graft recipient. 2. To test more extensively for suppressor cells in the long-term recipients, assessing lymphocytes in different immunological compartments and of different functional phenotypes. The suppression of mixed lymphocyte culture generation of lymphocyte mediated cytotoxicity, and the in vivo reconstitution of immune responsiveness, will be employed. 3. A careful analysis for anti-donor, or anti-host-idiotype, antibody as a possible mechanism of suppression will be done using an ELISA assay. 4. The possibility that there has been a change in the antigenicity of the heart grafts will be studied by determining the fate of retransplanted hearts, and by assessing the Ia antigen content of the healthy graft surviving long-term.
