Xenograft rejection: IgG1, complement and NK cells team up to activate and destroy the endothelium.
Acute vascular rejection represents a formidable barrier to clinical xenotransplantation and it is known that this type of rejection can also be initiated by xenoreactive antibodies that have limited complement-activating ability. Using a sophisticated mouse model, a recent study has provided in vivo evidence for the existence of an IgG(1)-mediated vascular rejection, which uniquely depends on both the activation of complement and interactions with FcgammaRIII on natural killer (NK) cells.
Rieben
Robert
R
Department of Clinical Research, University of Bern, Murtenstrasse 31, PO Box 33, CH-3010 Bern, Switzerland. robert.rieben@dkf.unibe.ch
Seebach
Jörg D
JD
D000818:Animals; D003167:Complement Activation / Q000276:immunology; D004727:Endothelium / Q000276:immunology*; D006084:Graft Rejection / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology* / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D014183:Transplantation, Heterologous / Q000276:immunology*
D007074:Immunoglobulin G