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Updated: Aug 20, 2026

Xenograft Skin Model to Manipulate Human Immune Responses In Vivo
Published on: June 29, 2022
Xenograft rejection: IgG1, complement and NK cells team up to activate and destroy the endothelium
Robert Rieben1, Jörg D Seebach
1Department of Clinical Research, University of Bern, Murtenstrasse 31, PO Box 33, CH-3010 Bern, Switzerland. robert.rieben@dkf.unibe.ch
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.
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.
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