title: Enhanced expression levels of IL-31 correlate with IL-4 and IL-13 in atopic and allergic contact dermatitis.
abstract: BACKGROUND
  IL-31 is produced by activated T lymphocytes, preferentially by TH2 cells. Transgenic mice overexpressing IL-31 have a phenotype resembling allergic dermatitis in human subjects.
  
  
  OBJECTIVE
  We sought to evaluate the potential importance of IL-31 in the pathogenesis of human T cell-mediated skin diseases.
  
  
  METHODS
  We analyzed total RNA taken from 149 skin biopsy specimens from patients with atopic dermatitis (AD), allergic contact dermatitis (ACD), or psoriasis in comparison with specimens taken from patients with healthy skin (n = 13) by using quantitative real-time PCR for the expression of TH1/TH2 cytokines.
  
  
  RESULTS
  We found statistically increased mRNA levels of IL-31 in biopsy specimens taken from patients with AD, irrespective of the severity of the disease and serum IgE levels. Moreover, IL-31 mRNA levels were strongly increased in many biopsy specimens taken from patients with ACD. However, no increased transcription of IL-31 could be detected in biopsy specimens taken from psoriatic plaques. A comparison of mRNA levels of IL-31 with TH1 or TH2 cytokines demonstrates a correlation of the expression of IL-31 with IL-4 and IL-13 but not with IFN-gamma. No significant increase of IL-31 receptor mRNA could be detected in any disease, whereas the second receptor subunit of IL-31, the oncostatin M receptor, seems to be enhanced transcribed in patients with psoriasis.
  
  
  CONCLUSIONS
  IL-31 expression is not only increased in patients with AD but also in those with ACD, 2 pruritic skin disorders. In both types of eczema, expression of IL-31 is associated with the expression of the TH2 cytokines IL-4 and IL-13.
  
  
  CONCLUSIONS
  IL-31 might contribute not only to the development of AD but also to ACD-provoked skin inflammation.
authors.affiliation: Department of Dermatology and Allergology, University Hospital RWTH Aachen, Germany.
authors.forename: Mark M
authors.initials: MM
authors.lastname: Neis
authors.forename: Bettina
authors.initials: B
authors.lastname: Peters
authors.forename: Alexandra
authors.initials: A
authors.lastname: Dreuw
authors.forename: Joerg
authors.initials: J
authors.lastname: Wenzel
authors.forename: Thomas
authors.initials: T
authors.lastname: Bieber
authors.forename: Cornelia
authors.initials: C
authors.lastname: Mauch
authors.forename: Thomas
authors.initials: T
authors.lastname: Krieg
authors.forename: Sven
authors.initials: S
authors.lastname: Stanzel
authors.forename: Peter C
authors.initials: PC
authors.lastname: Heinrich
authors.forename: Hans F
authors.initials: HF
authors.lastname: Merk
authors.forename: Andreas
authors.initials: A
authors.lastname: Bosio
authors.forename: Jens M
authors.initials: JM
authors.lastname: Baron
authors.forename: Heike M
authors.initials: HM
authors.lastname: Hermanns
mesh_terms: D017449:Dermatitis, Allergic Contact / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000276:immunology*; D005260:Female; D015870:Gene Expression; D020869:Gene Expression Profiling; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D018793:Interleukin-13 / Q000096:biosynthesis*; D015847:Interleukin-4 / Q000096:biosynthesis*; D007378:Interleukins / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014158:Transcription, Genetic
chemical_list: C502187:IL31 protein, human; D018793:Interleukin-13; D007378:Interleukins; D012333:RNA, Messenger; D015847:Interleukin-4; D007073:Immunoglobulin E