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Originally published In Press as doi:10.1074/jbc.M200419200 on April 30, 2002

J. Biol. Chem., Vol. 277, Issue 30, 27535-27544, July 26, 2002
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Opposite Regulation of Type II and III Receptors for Immunoglobulin G in Mouse Glomerular Mesangial Cells and in the Induction of Anti-glomerular Basement Membrane (GBM) Nephritis*

Heinfried H. RadekeDagger §, Iska Janssen-Graalfs||, Eveline N. SowaDagger ||, Nelli Chouchakova, Julia Skokowa, Fabian Löscher, Reinhold E. Schmidt, Peter Heeringa**, and J. Engelbert GessnerDagger Dagger

From the  Department of Clinical Immunology and Dagger  Institute of Pharmacology, Medical School of Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany, § Pharmazentrum Frankfurt, Clinic of Goethe University, 60590 Frankfurt, Germany, and ** Department of Immunology, University of Maastricht, 6221 ER Maastricht, The Netherlands

We examined the capacity of mouse glomerular mesangial cells (MC) to express and function through two different low affinity Fcgamma Rs, the activating Fcgamma RIII and the inhibitory Fcgamma RII. Immunohistochemistry identified Fcgamma RII as the prominent Fcgamma R in the kidney, and low levels of Fcgamma RIIb2-specific mRNA were also detected in primary cultures of growth-arrested MC. Activation by tumor necrosis factor-alpha /interleukin-1beta induced substantial Fcgamma RII expression in proliferating MC. Importantly, however, stimulation with interferon-gamma (IFN-gamma )/lipopolysaccharide or IFN-gamma alone resulted in a complete down-regulation of Fcgamma RII, which was accompanied by a strong increase in FcRgamma chain mRNA and a surface appearance of Fcgamma RIII. Activating Fcgamma RIII triggered mRNA synthesis for monocyte chemoattractant protein-1 (MCP-1), MCP-5, cytokine-induced neutrophil chemoattractant, and RANTES, whereas Fcgamma RIII-deficient MC failed to respond to immune complex (IC) activation as shown by impaired production of MCP-1 mRNA/protein. In a passive model of acute anti-glomerular basement membrane (GBM) nephritis, induction of Fcgamma RIII and suppression of Fcgamma RII occurred in kidney tissues. Blockade of Fcgamma RII, when induced selectively in the kidney, resulted in enhanced inflammation. Taken together, our results define a novel regulatory pathway with opposite regulation of Fcgamma RII (suppressed) and Fcgamma RIII (induced) by IFN-gamma on MCs in vitro and anti-GBM IgG in vivo. Herein is provided the first evidence that glomerular Fcgamma RII plays an important immunoregulatory role in the initiation of IC glomerulonephritis.

* This work was supported in part by Grants Ge892/5-1 and Ge892/7-2 from the Deutsche Forschungsgemeinschaft (to J. E. G.) and by Medizinische Hochschule Hannover Graduate Program funding (for E. N. S.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| These authors contributed equally to this work.

Dagger Dagger To whom correspondence should be addressed: Abteilung für Klinische Immunologie, Medizinische Hochschule Hannover, CarlNeuberg-Str. 1, 30625 Hannover, Germany. Tel.: 49-511-532-3621; Fax:49-511-532-5648; E-mail: Gessner.Johannes@MH-Hannover.de.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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