Mechanisms of tissue injury in hyperacute xenograft rejection.
Vascularized organs transplanted between phylogenetically distant species are subject to hyperacute rejection. The pathologic features of hyperacute rejection appear to be caused by profound dysfunction of small blood vessels in the graft. The author describes a model for the initiation and pathogenesis of hyperacute rejection. The model focuses on the endothelial cell as a target of the recipient immune reaction. Rejection is initiated by the binding to donor endothelial cells of recipient xenoreactive natural antibodies, which, in turn, triggers the complement cascade. These events lead to activation of graft endothelial cells, which promotes the thrombus formation and loss of vascular integrity characteristic of hyperacute rejection.
Platt
J L
JL
Department of Pediatrics, University of Minnesota, Minneapolis 55455.
D000818:Animals; D003167:Complement Activation / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology*; D006084:Graft Rejection / Q000276:immunology*; D006801:Humans; D008954:Models, Biological; D013927:Thrombosis / Q000209:etiology; D014181:Transplantation Immunology; D014183:Transplantation, Heterologous / Q000276:immunology / Q000473:pathology*