Avxr Versus Acute Vascular Allograft Rejection Avar

The fundamental role of the xenoantibody-aGal interaction in pig-to-primate AVXR is best supported by the fact that an almost identical interaction occurring in ABO incompatible allotransplantation is undeniably the initiating event in a rejection process which closely resembles AVXR. Human grafts transplanted into ABO incompatible recipients undergo an acute vascular allograft rejection (AVAR) which resembles the AVXR seen when hCRP transgenic pig xenografts are transplanted into primates. In both situations, the donor's complement regulatory mechanisms are functional and therefore MAC formation is inhibited. Strategies that have been successful in prolonging ABO incompatible allograft survival have also been successful in prolonging xenograft survival. However, the cross-species regulatory incompatibilities implicated in AVXR, clearly do not play a role in AVAR. The two primary ABO blood group antigens, A and B, are terminal endothelial carbohydrates similar to aGal. Since these antibody-ABO antigen interactions independently initiate AVAR, the almost identical xenoantibody-aGal interaction which occurs in pig-to-primate xenotransplantation is likely sufficient to initiate AVXR, without contribution from other mechanisms. Therefore, while other mechanisms may contribute to AVXR, the xenoantibody-aGal interaction likely plays a central role in its initiation.

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