Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors.

Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors. Research Abstract Details 

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Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors. Abstract Text:

Jin Wen Ding,Tingting Zhou,Huasong Zeng,Lianli Ma,J Sjef Verbeek,Dengping Yin,Jikun Shen,Anita S Chong,Jin Wen Ding,Tingting Zhou,Huasong Zeng,Lianli Ma,J Sjef Verbeek,Dengping Yin,Jikun Shen,Anita S Chong,

We have previously reported that anti-Gal-alpha1,3Gal (Gal) IgG3 mAbs mediate a classical complement-dependent hyperacute rejection (HAR), while anti-Gal IgG1 mAbs mediate HAR that is dependent on complement, the Fc-gamma receptors FcgammaRII/III (CD32/CD16), and NK cells. IgG2a and IgG2b subclasses can activate complement and have FcgammaR binding properties in vitro. Whether these IgG subclasses can mediate HAR in vivo and the mechanisms by which they would do so are not known. In this study, we isolated spontaneous IgG switch mutants from an anti-Gal IgG1 hybridoma. In vitro complement-mediated hemolytic assays with mouse complement indicate that both anti-Gal IgG2a and IgG2b mAbs were more potent compared with the parent anti-Gal IgG1. In vivo administration of anti-Gal IgG2a and IgG2b mAbs into Gal(-/-) mice induced HAR of rat cardiac xenografts. HAR induced by anti-Gal IgG2a and IgG2b was dependent on complement activation and the presence of NK cells. Using FcgammaRIII-deficient (Gal(-/-)CD16(-/-)) recipients, we observed that HAR mediated by different anti-Gal IgG subclasses was variably dependent on FcgammaRIII, with IgG1 > IgG2b >> IgG2a = IgG3. Using FcgammaRI-deficient (Gal(-/-)CD64(-/-)) recipients, we observed that HAR mediated by anti-Gal IgG1, IgG2a, and IgG2b, but not by anti-Gal IgG3, was dependent on FcgammaRI. Collectively, these studies demonstrate the necessity and sufficiency of complement in IgG3-mediated HAR and the necessity of both complement and FcgammaR, especially FcgammaRI, in IgG1-, IgG2a-, and IgG2b-mediated HAR.

Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors. Publishing Authors By Initials

JW Ding,T Zhou,H Zeng,L Ma,JS Verbeek,D Yin,J Shen,AS Chong,JW Ding,T Zhou,H Zeng,L Ma,JS Verbeek,D Yin,J Shen,AS Chong,

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Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 180

Page Numbers: 261-8

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Jan

YEAR: 2008

Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors. Information

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LANGUAGE: eng

NlmUniqueID: 2985117

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Grant and Affiliation Information for Hyperacute Rejection by Anti-Gal IgG1, IgG2a, and IgG2b Is Dependent on Complement and Fc-{gamma} Receptors.

AFFILIATION: Section of Transplantation, Department of Surgery, University of Chicago, Chicago, IL 60637.

Country: United States

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MEDLINETA: J Immunol

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