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Rheumatology 2006 45(Supplement 3):iii14-iii16; doi:10.1093/rheumatology/kel284
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Pathophysiology of cutaneous lupus erythematosus — novel aspects

A. Kuhn1,2,, P. H. Krammer2 and V. Kolb-Bachofen3

1Department of Dermatology, University of Düsseldorf, Düsseldorf, 2Institute of Immunogenetics, Tumor Immunology Program, German Cancer Research Center, Heidelberg and 3Research Group Immunobiology, University of Düsseldorf, Düsseldorf, Germany.

Correspondence to: Annegret Kuhn, MD, Institute of Immunogenetics, Tumor Immunology Program, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany. E-mail: kuhnan{at}uni-duesseldorf.de

The pathophysiology of cutaneous lupus erythematosus (CLE) has been investigated in numerous studies demonstrating that the combination of specific cellular and molecular events is leading to inflammation and tissue damage in this disease. However, a complete understanding of the diverse pathophysiological mechanisms and interactions does not exist. Various environmental factors influence the clinical expression of CLE and a striking relationship has emerged between sunlight exposure and the various subtypes of this disease. In the past years, photoprovocation tests with different ultraviolet (UV) wavelengths have been approved to be an optimal way to evaluate photosensitivity in patients with CLE. Furthermore, research on the pathogenetic mechanisms of UV-induced skin lesions has become an increasingly dynamic field and several new aspects of this disease could be identified. In this review, the impact of UV exposure that contributes to the manifestations of CLE is discussed and recently reported mechanisms in the pathophysiology of this disease are considered including the clearance of apoptotic cells, expression of inducible nitric oxide synthase, function of CD4+CD25+ regulatory T cells, and the role of chemokines for lymphocyte recruitment. Elucidation of the relevant factors might lead to future development of effective strategies to prevent abnormal reactivity in patients with CLE.


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