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Lymphocyte subtypes and adhesion molecules in actinic prurigo: observations with cyclosporin A
Author(s) -
Umaña Angela,
Gómez Alberto,
Durán María Mélida,
Porras Luisa
Publication year - 2002
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1046/j.1365-4362.2002.01419.x
Subject(s) - medicine , cell adhesion molecule , photodermatosis , prurigo , intercellular adhesion molecule 1 , cd8 , antigen , adhesion , immunology , human leukocyte antigen , lymphocyte , hla dr , pathology , dermatology , chemistry , dna , biochemistry , organic chemistry , xeroderma pigmentosum , dna damage
Background Actinic prurigo is a photodermatitis in which UV light is implicated by an unknown mechanism. Methods Skin biopsies of 19 patients with actinic prurigo and 11 controls were analyzed by immunohistochemistry. Results In actinic prurigo patients, there was a significant increase in the number of CD3, CD4, CD8, CD45RA, CD45RO, and CD45RB lymphocytes and Langerhans cells, as well as in the level of human leukocyte antigen‐DR (HLA‐DR) expression and cell adhesion molecules lymphocyte functional antigen‐1 (LFA‐1), intercellular adhesion molecule‐1 (ICAM‐1), and endothelial leukocyte adhesion molecule‐1 (ELAM‐1). Actinic prurigo patients were treated with cyclosporin A (CsA), and a final skin biopsy was taken after 6 months of treatment. All the cell populations and markers studied, except for the CD4 lymphocytes, Langerhans cells, and HLA‐DR expression, returned to normal levels. Conclusions CsA was found to be effective in relieving the clinical symptoms of actinic prurigo.