Patients will be followed closely in the post transplant period for evidence of a detrimental immune response to the allograft. In the previous patients experiencing graft directed immunity the graft dysfunction was preceded by a rise in activated monocytes in the peripheral blood and augmented transcription of the cytokine Tumor Necrosis Factor-alpha (TNF-a) in the allograft. This syndrome has been resistant to treatment with the TNF-a sequestrant Infliximab and is now thought to require more comprehensive monocyte directed therapy. If patients progress and graft dysfunction occurs, patients will be treated with methylprednisolone and have immunosuppression added using sirolimus as the predominant immunosuppressive agent. This maneuver has in all cases been successful in returning the allograft to normal function. Sirolimus has been chosen since it does not act by interfering with specific T cell receptor function, and thus, provides immunosuppressive coverage during cell repopulation without interfering with the antigen specific T cell events important for tolerance induction. Non-human primate and human clinical data support both of these approaches.