Abstract
NUMEROUS studies have focused on the pig-to-primate model because of its clinical relevance. This model has allowed the definition of mechanisms of rejection initiated by the binding of the recipient's xenoreactive natural antibodies (XNA) that react with the donor graft endothelial cells (ECs) and activate the complement (C). 1,2 The generation of transgenic pigs with modified properties is a promising approach to overcome hyperacute rejection (HAR) of xenograft. However, the production of large transgenic animals such as pigs is a costly and time-consuming process, as compared to small laboratory animals such as rats. We developed a rat-to-primate cardiac xenograft model as an alternative to assess more rapidly the efficiency of strategies for preventing xenograft rejection. 3 In this model, HAR was obtained after 5.5 ± 1.4 minutes and mediated by the same physiopathologic mechanisms as in the pig-to-primate combination, in particular for the binding of XNA and C activation. The Galα(1,3)Gal epitope is the major xenoantigen in pigs. 4 The aim of this work was to study its role in the rat-to-primate combination.
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