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

Dengping Yin, Huasong Zeng, Lianli Ma, Jikun Shen, Hui Xu, Guerard W. Byrne, Anita S. Chong

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


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-α1,3Gal (Gal) IgG1, with modest complement-activating abilities in vitro, to induce xenograft rejection. This rejection was dependent on the activation of complement, on FcγR-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, FcγR, and NK cells.

Original languageEnglish (US)
Pages (from-to)7235-7238
Number of pages4
JournalJournal of Immunology
Issue number12
StatePublished - Jun 15 2004
Externally publishedYes


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