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Profile of cytokine mRNA expression in spontaneous and UV‐induced skin lesions from actinic prurigo patients
Author(s) -
SantosMartínez L.,
Llorente L.,
Baranda L.,
RichaudPatin Y.,
TorresAlvarez B.,
Moncada B.,
GonzálezAmaro R.
Publication year - 1997
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1997.tb00153.x
Subject(s) - cytokine , medicine , photodermatosis , prurigo , immunology , interleukin 6 , dermatology , pathology , chemistry , gene , xeroderma pigmentosum , biochemistry , dna repair
Background – Actinic prurigo (AP) appears to be an immunemediated disease triggered by exposure to ultraviolet light (UV). Objective – To assess the profile of cytokine production in skin lesions from AP patients. Methods – The cytokine production (IL‐1β 1L‐2, IL‐4. IL‐6. IL‐I0. 1L‐I3, TNF‐α, IFN‐τ, and TGF‐β) in skin biopsies from 12 AP lesions was determined by a semiquantitative coupled reverse transcription‐poly‐merase chain reaction. Result – We found expression of TGF‐β and 1L‐13 genes in most AP skin lesions; IL‐lβ. IL‐6. TNF‐α. IFN‐τ. and IL.‐10 were detected in some of these specimens. However, the levels of expression of all cytokines studied were not significantly different in AP skin lesions compared to nonlesional skin. Conclusions TGF‐β and IL‐13 might have a key role in both the inflammatory phenomenon and absence of significant expression of most cytokines in AP skin. The cytokine production in AP skin resembles that observed in rheumatoid synovium. a paucity in cytokine expression despite the presence of infiltrating activated mononuclcar cells.