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NDT Advance Access published online on August 31, 2004
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfh459
© 2004 by European Renal Association - European Dialysis and Transplant Association
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Received December 24, 2003
Accepted July 15, 2004

Original Article

Injection of recombinant Fc{alpha}RI/CD89 in mice does not induce mesangial IgA deposition

Paul J. M. van der Boog 1*, Cees van Kooten 1, Ger van Zandbergen 1, Ngaisah Klar-Mohamad 1, Beatrijs Oortwijn 1, Nico A. Bos 2, Alexandra van Remoortere 3, Cornelis H. Hokke 3, Johan W. de Fijter 1, Mohamed R. Daha 1

1 Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands
2 Department of Cell Biology, University of Groningen, The Netherlands
3 Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands

* To whom correspondence should be addressed. E-mail: p.j.m.van_der_boog{at}lumc.nl.



  Abstract

Background. Earlier studies have suggested that complexes of the human IgA receptor Fc{alpha}RI/CD89 with mouse IgA are pathogenic upon deposition in the renal mesangium. Transgenic mice expressing Fc{alpha}RI/CD89 on macrophages/monocytes developed massive mesangial IgA deposition and a clinical picture of IgA nephropathy (IgAN). Based on these findings, the purpose of this study was to design an experimental model of IgAN by injection of human CD89 in mice. The interaction of mouse IgA with CD89 was investigated further.

Methods. Recombinant human soluble CD89 and a chimeric CD89-Fc protein were generated, produced, purified and injected in mice. Renal cryosections were stained for IgA and CD89. The interaction of mouse IgA with CD89 was analysed by fluorescence-activated cell sorting (FACS) analysis, enzyme-linked immunosorbent assay (ELISA) and plasmon resonance technology.

Results. Injection of recombinant human CD89 did not result in significant IgA or CD89 deposition in the renal mesangium. However, CD89 staining in the liver was found to be positive. CD89 was rapidly cleared from circulation without signs of complex formation with IgA. FACS analysis, ELISA and plasmon resonance techniques all revealed a dose-dependent binding of human IgA to recombinant CD89, while no detectable binding was seen of mouse IgA, either of serum IgA or of different monoclonal mouse IgA preparations.

Conclusions. An experimental model for IgAN in mice could not be obtained by injection of recombinant CD89. This is compatible with our in vitro biochemical data showing a lack of binding between recombinant human CD89 and mouse IgA.

Keywords: CD89; IgA; IgA nephropathy; mouse; receptor.
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