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Rheumatology Advance Access published online on May 31, 2005
Rheumatology, doi:10.1093/rheumatology/keh693
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received March 8, 2005
Accepted April 26, 2005

6th European Lupus Meeting

SLE--a disease of clearance deficiency?

L. E. Munoz 1, U. S. Gaipl 1, S. Franz 1, A. Sheriff 1, R. E. Voll 2, J. R. Kalden 1, and Martin Herrmann 1*

1 Institute for Clinical Immunology, Department of Medicine III, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany
2 IZKF Research Group N2, Nikolaus-Fiebiger Center of Molecular Medicine, Erlangen, Germany

* To whom correspondence should be addressed.
Martin Herrmann, E-mail: martin.herrmann{at}med3.imed.uni-erlangen.de


  Abstract

Systemic lupus erythematosus (SLE) is a multifactorial disease and its pathogenesis and precise aetiology remain unknown. Under physiological conditions, neither apoptotic nor necrotic cell material is easily found in tissues because of its quick removal by a highly efficient scavenger system. Autoantigens are found in apoptotic and necrotic material and they are recognized by autoimmune sera from SLE patients. The clearance of dying cells is finely regulated by a highly redundant system of receptors on phagocytic cells and bridging molecules, which detect molecules specific for dying cells. Changes on apoptotic and necrotic cell surfaces are extremely important for their recognition and further disposal. Some SLE patients seem to have an impaired ability to clear such apoptotic material from tissues, and this could cause the breakdown of central and peripheral mechanisms of tolerance against self-antigens. In this article, we address the cells, receptors and molecules involved in the clearance process and show how deficiencies in this process may contribute to the aetiopathogenesis of SLE.

Keywords: Apoptosis; Necrosis; Phagocytosis; Clearance; Autoimmunity; SLE.
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