The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
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Published online 27 March 2006 doi:10.1084/jem.20052367
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 4, 953-960
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ARTICLE

Impaired Langerhans cell migration in psoriasis

Marie Cumberbatch1, Minal Singh2, Rebecca J. Dearman1, Helen S. Young2, Ian Kimber1, and Christopher E.M. Griffiths2

1 Syngenta Central Toxicology Laboratory, Macclesfield, Cheshire, SK10 4TJ, England, UK
2 The Dermatology Centre, University of Manchester, Salford, Manchester, M6 8HD, England, UK

CORRESPONDENCE Christopher E.M. Griffiths: Christopher.griffiths{at}manchester.ac.uk

We have examined whether psoriasis is associated with systemic effects on epidermal Langerhans cell (LC) function and, specifically, the migration of LCs from the skin. Compared with normal skin, the frequency and morphology of epidermal LCs in uninvolved skin from patients with psoriasis was normal. However, mobilization of these cells in response to stimuli that normally induce migration (chemical allergen, tumor necrosis factor {alpha} [TNF-{alpha}], and interleukin-1ß [IL-1ß]) was largely absent, despite the fact that treatment with TNF-{alpha} and IL-1ß was associated with comparable inflammatory reactions in patients and controls. The failure of LC migration from uninvolved skin was not attributable to altered expression of receptors for IL-1ß or TNF-{alpha} that are required for mobilization, nor was there an association with induced cutaneous cytokine expression. Although a role for altered dynamics of LC migration/turnover has not been formally excluded, these data reveal a very consistent decrement of LC function in psoriasis that may play a decisive role in disease pathogenesis.


Abbreviations used: LC, Langerhans cell; DPC, diphenylcyclopropenone; IL-1Ra, IL-1R antagonist; PDC, plasmacytoid DC.


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