Abstract
HE COMPLEMENT system has been shown to play a central pathophysiologic role in hyperacute rejection (HAR) 1 and to contribute to the inflammation and organ injury associated with transplantation. 2 Recently, a novel phage-displayed C3-binding peptide (Compstatin) has been identified that suppresses complement activation and therefore may be of therapeutic value in clinical situations such as xenotransplantation that involve complement-mediated tissue damage. This peptide binds reversibly to the C3c portion of native C3 and inhibits both the classical and alternative pathways of complement activation. 3 Our results
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