We have previously demonstrated that a kidney allograft has the ability to confer tolerance on a co-transplanted heart allograft procured from a class I-mismatched donor. However, kidney-induced cardiac allograft tolerance (KICAT) has not been tested in a fully MHC-disparate strain combination. The purpose of this study was to determine whether tolerance could be induced in heart/kidney transplant recipients across a more clinically relevant full-MHC barrier. Heart allografts (n=3) or heart/kidney allografts (n=5) were transplanted heterotopically into fully mismatched recipients that were treated with high-dose tacrolimus for 12 days. All isolated heart allografts rejected by POD 40. In contrast, all heart/kidney allografts survived for >100 days, with no evidence of rejection on serial cardiac biopsies. Heart/kidney recipients lost donor-specific responsiveness in CML and MLR assays, and did not develop alloantibody. These results show that KICAT can be extended to fully mismatched allografts in a consistent and robust manner. Elucidating the renal element responsible for KICAT could provide mechanistic information that leads to protocols aimed at inducing tolerance in recipients of isolated heart allografts.
To cite this abstract in AMA style:Madariaga M, Michel S, Tasaki M, Villani V, Farkash E, La G, Allan J, Sachs D, Yamada K, Madsen J. Kidney-Induced Cardiac Allograft Tolerance across a Full MHC-Barrier in Miniature Swine [abstract]. Am J Transplant. 2013; 13 (suppl 5). http://atcmeetingabstracts.com/abstract/kidney-induced-cardiac-allograft-tolerance-across-a-full-mhc-barrier-in-miniature-swine/. Accessed September 24, 2017.
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