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NDT Advance Access originally published online on September 22, 2008
Nephrology Dialysis Transplantation 2008 23(12):3771-3772; doi:10.1093/ndt/gfn536
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Proteasome inhibition: a new therapeutic option in lupus nephritis?*

Johan van der Vlag and Jo H. M. Berden

Nephrology Research Laboratory Nijmegen Center for Molecular Life Sciences, Division of Nephrology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands

Correspondence and offprint requests to: Jo H. M. Berden, Division of Nephrology (464), Radboud University Nijmegen Medical Center, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Tel: +31-24-3614761; Fax: +31-24-3540022; E-mail: j.berden@nier.umcn.nl

Keywords: B cells; bortezomib; lupus nephritis; lupus; proteasome

The first 10% of the full text of this article appears below.

Antinuclear auto-antibodies are a hallmark of systemic lupus erythematosus. Based on the characteristics of these auto-antibodies (somatic mutation, restricted use of certain VH and VL genes, high avidity IgG antibodies, common idiotypes), lupus is regarded as an auto-antigen-driven T-cell-dependent autoimmune disease [1]. It is generally assumed, however, that the produced auto-antibodies are pivotal for the development of tissue lesions, and hence also B cells are necessary for disease development. Indeed, MRL/lpr lupus mice, which due to a certain genetic manipulation lack B cells, develop neither glomerulonephritis nor vasculitis [2]. Therefore, in lupus, B cells represent a major target . . . [Full Text of this Article]


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