title: T cell phenotype in allergic asthma and atopic dermatitis.
abstract: BACKGROUND
  T cells are key regulators of immunologic disease parameters. However, their contribution to the process of tissue remodeling is ill defined. In the present study, we investigated gene expression of allergy-characteristic, IL-4-rich T cell cDNAs to monitor expression of genes that might participate in the pathogenesis of allergic diseases.
  
  
  METHODS
  cDNAs of freshly isolated and restimulated CD4+ T cells from patients with allergic asthma (AA) or atopic dermatitis (AD) and healthy subjects were analyzed on Nylon membrane-based DNA arrays. Three patients were selected for an allergy-characteristic T cell phenotype with high IL-4 expression (AA) or IL-13 expression (AD).
  
  
  RESULTS
  Several gene families such as the TGF-beta family, chemokines and chemokine receptors were found to be upregulated. Matrix metalloproteinases and their inhibitors were also found to be expressed in an enhanced manner. Furthermore, factors regulating tissue turnover such as fibroblast growth factors and neurotrophic as well as vasoactive factors were found be expressed at a higher level in allergic patient compared to healthy donors.
  
  
  CONCLUSIONS
  The present study reveals and confirms genes relevant for allergy and highlights an approach to applying a DNA array technique for diagnostic discrimination of allergic diseases.
authors.affiliation: Swiss Institute of Allergy and Asthma Research (SIAF), Davos, Switzerland.
authors.forename: Jan G
authors.initials: JG
authors.lastname: Wohlfahrt
authors.forename: Steffen
authors.initials: S
authors.lastname: Kunzmann
authors.forename: Günther
authors.initials: G
authors.lastname: Menz
authors.forename: Werner
authors.initials: W
authors.lastname: Kneist
authors.forename: Cezmi A
authors.initials: CA
authors.lastname: Akdis
authors.forename: Kurt
authors.initials: K
authors.lastname: Blaser
authors.forename: Carsten B
authors.initials: CB
authors.lastname: Schmidt-Weber
mesh_terms: D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000502:physiology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D019334:Endothelin-3 / Q000096:biosynthesis / Q000235:genetics; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D018793:Interleukin-13 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D020782:Matrix Metalloproteinases / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D020411:Oligonucleotide Array Sequence Analysis; D016133:Polymerase Chain Reaction; D012313:RNA / Q000737:chemistry / Q000235:genetics; D019707:Receptors, Chemokine / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D019714:Tissue Inhibitor of Metalloproteinases / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines; D019334:Endothelin-3; D018793:Interleukin-13; D019707:Receptors, Chemokine; D019714:Tissue Inhibitor of Metalloproteinases; D016212:Transforming Growth Factor beta; D015847:Interleukin-4; D012313:RNA; D020782:Matrix Metalloproteinases