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Characterization of the interleukin‐17 isoforms and receptors in lesional psoriatic skin
Author(s) -
Johansen C.,
Usher P.A.,
Kjellerup R.B.,
Lundsgaard D.,
Iversen L.,
Kragballe K.
Publication year - 2009
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2008.08902.x
Subject(s) - psoriasis , receptor , gene isoform , messenger rna , interleukin , cytokine , interleukin 17 , keratinocyte , proinflammatory cytokine , interleukin 23 , biology , inflammation , immunology , medicine , microbiology and biotechnology , cell culture , gene , biochemistry , genetics
Summary Background  Th17 cells are a lineage of proinflammatory T helper cells producing interleukin (IL)‐17. The importance of Th17 cells in inflammation and autoimmunity has now been recognized. The IL‐17 cytokine family consists of six isoforms (IL‐17A–IL‐17F) whereas five members of the IL‐17 receptor (IL‐17R) family have been identified (IL‐17RA–IL‐17RE). Objectives  To characterize the expression of the IL‐17 isoforms and receptors in lesional and nonlesional psoriatic skin. Methods  Keratome and punch biopsies taken from patients with psoriasis were examined by enzyme‐linked immunosorbent assay and quantitative reverse transcription–polymerase chain reaction in order to measure the IL‐17 isoforms and receptors. Results  We demonstrated significantly increased mRNA expression of IL‐17A, IL‐17C and IL‐17F in psoriatic skin. In contrast, the mRNA expression of IL‐17B and IL‐17D was significantly decreased in lesional compared with nonlesional skin, while IL‐17E mRNA was undetectable. The increased mRNA expression of IL‐17A, IL‐17C and IL‐17F was paralleled by an increased protein accumulation of these cytokines in psoriatic skin. Analysis of the IL‐17R mRNA expression revealed significantly impaired mRNA expression of IL‐17RB, IL‐17RC, IL‐17RD and IL‐17RE in lesional psoriatic skin, whereas the mRNA expression of IL‐17RA was similar in lesional and nonlesional psoriatic skin. Conclusions  This study characterizes the mRNA profile of the IL‐17 isoforms and receptors in psoriatic skin lesions. Furthermore, we demonstrate for the first time augmented protein levels of IL‐17A, IL‐17C and IL‐17F in psoriatic skin lesions, indicating a possible role for IL‐17C in addition to IL‐17A and IL‐17F in the pathogenesis of psoriasis.

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