Pathology and protection in nephrotoxic nephritis is determined by selective engagement of specific Fc receptors

The Journal of Experimental Medicine
Yoshikatsu KanekoJ V Ravetch

Abstract

Introduction of heterologous anti-glomerular basement membrane antiserum (nephrotoxic serum, NTS) into presensitized mice triggers the production of IgG anti-NTS antibodies that are predominantly IgG2b and the glomerular deposition of pathogenic immune complexes, leading to accelerated renal disease. The pathology observed in this model is determined by the effector cell activation threshold that is established by the coexpression on infiltrating macrophages of the IgG2a/2b restricted activation receptor FcgammaRIV and its inhibitory receptor counterpart, FcgammaRIIB. Blocking FcgammaRIV with a specific monoclonal antibody thereby preventing IgG2b engagement or treatment with high dose intravenous gamma-globulin (IVIG) to down-regulate FcgammaRIV while up-regulating FcgammaRIIB, protects mice from fatal disease. In the absence of FcgammaRIIB, IVIG is not protective; this indicates that reduced FcgammaRIV expression alone is insufficient to protect animals from pathogenic IgG2b immune complexes. These results establish the significance of specific IgG subclasses and their cognate FcgammaRs in renal disease.

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Citations

Feb 25, 2010·Annals of Hematology·Markus BiburgerFalk Nimmerjahn
Sep 6, 2006·Springer Seminars in Immunopathology·Lucie BaudinoShozo Izui
Nov 23, 2006·Springer Seminars in Immunopathology·Falk Nimmerjahn
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Methods Mentioned

BETA
ELISA
flow cytometry
light microscopy

Software Mentioned

MetaMorph
SPSS

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