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IL-31 expression by inflammatory cells is preferentially elevated in atopic dermatitis

Nobbe, S; Dziunycz, P; Mühleisen, B; Bilsborough, J; Dillon, S R; French, L E; Hofbauer, G F L (2012). IL-31 expression by inflammatory cells is preferentially elevated in atopic dermatitis. Acta Dermato-Venereologica, 92(1):24-28.

Abstract

Interleukin-31 (IL-31) is a recently discovered cytokine expressed in many human tissues, and predominantly by activated CD4+ T cells. IL-31 signals through a heterodimeric receptor consisting of IL-31 receptor alpha (IL-31RA) and oncostatin M receptor beta (OSMR). Earlier studies have shown involvement of IL-31 and its receptor components IL-31RA and OSMR in atopic dermatitis, pruritus and Th2-weighted inflammation at the mRNA level. The aim of this study was to investigate IL-31 protein expression in skin of such conditions. Immunohisto-chemical staining for IL-31, IL-31RA and OSMR was performed in formalin-fixed paraffin-embedded biopsy specimens. IL-31 expression was increased in the inflammatory infiltrates from skin biopsies taken from subjects with atopic dermatitis, compared with controls (p ≤ 0.05). IL-31, IL-31RA and OSMR protein immunoreactivity was not increased in biopsies from subjects with other Th2-weighted and pruritic skin diseases. Our results confirm, at the protein level, the relationship between IL-31 expression and atopic dermatitis. Our results do not support a general relationship between expression of IL-31/IL-31R and pruritic or Th2-mediated diseases.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Dermatology
Language:English
Date:1 November 2012
Deposited On:11 Feb 2012 19:36
Last Modified:07 Sep 2024 01:36
Publisher:Society for the Publication of Acta Dermato-Venereologica
ISSN:0001-5555 (P) 1651-2057 (E)
OA Status:Gold
Publisher DOI:https://doi.org/10.2340/00015555-1191
Official URL:http://www.medicaljournals.se/acta/content/?doi=10.2340/00015555-1191
PubMed ID:22041865
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