Cutting Edge: NK cells mediate IgG1-dependent hyperacute rejection of xenografts.

Yin D, Zeng H, Ma L, Shen J, Xu H, Byrne GW, Chong AS
J Immunol. 2004 172 (12): 7235-8

PMID: 15187097 · DOI:10.4049/jimmunol.172.12.7235

Classic hyperacute rejection is dependent on the activation of the terminal components of complement. Recently, xenoantibodies with limited abilities to activate the classical pathway of complement in vitro have been implicated in the acute vascular rejection of xenografts. It is unclear how these Abs affect their pathogenic activities in vivo. In this study, we demonstrate the ability of an anti-Gal-alpha1,3Gal (Gal) IgG1, with modest complement-activating abilities in vitro, to induce xenograft rejection. This rejection was dependent on the activation of complement, on FcgammaR-mediated interactions, and on the presence of NK cells. Inhibition of any one of these factors resulted in the abrogation of IgG1-mediated rejection. In contrast, an anti-Gal IgG3 mAb induced classic, hyperacute rejection that was solely dependent on complement activation. Our observations implicate two types of IgG-mediated rejection; one that is dependent on complement activation, and a second that is uniquely dependent on complement, FcgammaR, and NK cells.

MeSH Terms (15)

Animals Antibodies, Monoclonal Complement Activation Disaccharides Graft Rejection Heart Transplantation Immunoglobulin G Killer Cells, Natural Mice Mice, Inbred C57BL Mice, Knockout Rats Rats, Inbred Lew Receptors, IgG Transplantation, Heterologous

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