RESEARCH - Is disturbed clearance of apoptotic keratinocytes responsible for UVB-induced skin lesions in SLE?

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Is disturbed clearance of apoptotic keratinocytes responsible for

UVB-induced inflammatory skin lesions in systemic lupus erythematosus?

Esther Reefman1 , Marcelus CJM de Jong2 , Hilde Kuiper3 , Marcel F

Jonkman2 , Pieter C Limburg1 , Cees GM Kallenberg1 and Marc Bijl1

1Department of Rheumatology and Clinical Immunology, University Medical

Center Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen,

The Netherlands

2Department of Dermatology, University Medical Center Groningen, University

of Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands

3Department of Pathology and Laboratory Medicine, University Medical Center

Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen, The

Netherlands

Arthritis Research & Therapy 2006, 8:R156 doi:10.1186/ar2051

Published 2 October 2006

Abstract

Apoptotic cells are thought to play an essential role in the pathogenesis of

systemic lupus erythematosus (SLE). We hypothesise that delayed or altered

clearance of apoptotic cells after UV irradiation will lead to inflammation

in the skin of SLE patients. Fifteen SLE patients and 13 controls were

irradiated with two minimal erythemal doses (MEDs) of ultraviolet B light

(UVB). Subsequently, skin biopsies were analysed (immuno)histologically,

over 10 days, for numbers of apoptotic cells, T cells, macrophages, and

deposition of immunoglobulin and complement. Additionally, to compare

results with cutaneous lesions of SLE patients, 20 biopsies of lupus

erythematosus (LE) skin lesions were analysed morphologically for apoptotic

cells and infiltrate. Clearance rate of apoptotic cells after irradiation

did not differ between patients and controls. Influx of macrophages in

dermal and epidermal layers was significantly increased in patients compared

with controls. Five out of 15 patients developed a dermal infiltrate that

was associated with increased epidermal influx of T cells and macrophages

but not with numbers of apoptotic cells or epidermal deposition of

immunoglobulins. Macrophages were ingesting multiple apoptotic bodies.

Inflammatory lesions in these patients were localised near accumulations of

apoptotic keratinocytes similar as was seen in the majority of LE skin

lesions. In vivo clearance rate of apoptotic cells is comparable between SLE

patients and controls. However, the presence of inflammatory lesions in the

vicinity of apoptotic cells, as observed both in UVB-induced and in LE skin

lesions in SLE patients, suggests that these lesions result from an

inflammatory clearance of apoptotic cells.

Full text here:

http://arthritis-research.com/content/8/6/R156

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