Baboon-to-human liver transplantation

Background. Previous studies demonstrated that hearts from transgenic pigs expressing human decay-accelerating factor (hDAF) were not hyperacutely rejected when transplanted heterotopically into the abdomen of cynomolgus monkeys. This study examines orthotopic transplantation of hDAF transgenic pig hearts into baboon recipients. Methods. Orthotopic xenogeneic heart transplantation was performed using piglets, transgenic for hDAF, as donors. Ten baboons were used as recipients and were immunosuppressed with a combination of cyclophosphamide, cyclosporine, and steroids. Results. Five grafts failed within 18 hr without any histological signs of hyperacute rejection. Pulmonary artery thrombosis induced by a size mismatch was observed in two of these animals. The other three recipients died because of failure to produce even a low cardiac output and/or dysrhythmia. The remaining five animals survived between four and nine days. One animal died of bronchopneumonia on day 4. Three xenografts stopped beating on day 5 due to acute vascular rejection. The longest survivor was killed on day 9 with a beating, histologically normal xenograft, because of pancytopenia. Conclusions. The results reported here demonstrate that hDAF transgenic pig hearts are not hyperacutely rejected when transplanted into baboon recipients. Orthotopically transplanted transgenic pig hearts are capable of maintaining cardiac output in baboons. An optimum immunosuppressive regimen is the subject of ongoing research.

Orthotopic heart transplantation in a transgenic pig-to-primate model.

Xenoreactive natural antibodies (XNA) and complement (C) are thought to be the two major inciting factors that result in hyperacute rejection (HAR) of an immediately vascularized, discordant xenograft within minutes to a very few hours, with destruction and infarction of the transplanted organ. If recipients are modified by various experimental modalities, such as removal and suppression of XNAand C-mediated responses, thus avoiding HAR, the process of delayed xenograft rejection (DXR) with a significant vascular component still occurs after a delay of several days or, at the most, a few weeks (Bach et al. 1993). The end result in both instances is the invariable and unacceptable loss of xenografts, which currently limits application of xenotransplantation beyond experimental protocols. The mechanisms underlying DXR are far from clear but appear not necessarily to involve XNAand C-mediated responses as those noted in HAR. Moreover, DXR can occur without the prominent participation of T lymphocytes. One of us (FHB) has suggested that the final common pathogenic mechanisms underly-

Endothelial cell activation and thromboregulation during xenograft rejection.

Transplant Accommodation in Highly Sensitized Patients: A Potential Role for Bcl‐xL and Alloantibody

The complement system in xenotransplantation.

Xenograft adaptation is dependent on the presence of antispecies antibody, not prolonged residence in the recipient.

Prolonged survival of hamster to rat heart xenografts with cyclophosphamide therapy.

“The immediate reason for this revival of interest in xenotransplantation must at least partially stem from a belief, whether true or false, that some of the newer immunosuppressive agents offer better promise of controlling the xenograft reaction than the conventional agents used prior to 1980” (Frank Thomas in [1]).

Immunosuppression in Xenotransplantation

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Xenograft adaptation is dependent on the presence of antispecies antibody, not prolonged residence in the recipient.

Prolonged survival of hamster to rat heart xenografts with cyclophosphamide therapy.

Immunosuppression in Xenotransplantation