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LIVER xenografting implies that most of the complement (C) in the recipients will be produced by the graft. It is known that membrane-bound proteins have the property of homologous restriction; ie. they inhibit MAC-mediated lysis only when the terminal C components are from the same species as the cells on which these proteins are expressed.1 To test the hypothesis that this could be a mechanism of protection from hyperacute rejection, we transplanted hamster hearts into stable hamster-to-rat liver xenograft recipients (OLT). Minutes later, hyperimmune serum (HS) obtained from untreated hamster heart xenograft recipients was given intravenously (IV)—either unaltered or C-inactivated by heating at 56°C for 30 minutes. Survival of the hamster hearts is shown in Table 1. Different dilutions of absorbed sera were tested in their ability to lyse hamster or mouse lymphocytes in a C-dependent cytotoxicity assay. Hamster serum did not lyse hamster cells. While antihamster HS and normal rat serum produced efficient lysis of hamster lymphocytes, that produced by OLT serum was poor. In contrast, OLT serum caused efficient lysis of mouse target cells. In conclusion, the homology of C and target cells represents a novel mechanism of protection that the liver confers to other organs.