KNOCK OUT OF α1,3GALACTOSYLTRANSFERASE OR EXPRESSION OFα1,2FUCOSYLTRANSFERASE FURTHER PROTECTS CD55 AND CD59EXPRESSING MOUSE HEARTS IN AN EX VIVO MODEL OF XENOGRAFT REJECTION

Organs from transgenic animals with highlevel endothelial expression of the human complement regulatory factors CD55 and CD59 are significantly protected from human complementmediated injury. Elimination or reduction of the major xenoepitope αGal, achieved by knocking out theα1,3galactosyltransferase gene Gal KO or expressing humanα1,2fucosyltransferase H transferase or HTF, also affords protection, although to a lesser degree. In this study, we examined whether the protection provided by strong CD55 and CD59 expression can be augmented by the Gal KO or HTF modifications.