title: Predominance of type 2 cytokine-producing CD4+ and CD8+ cells in patients with atopic dermatitis.
abstract: BACKGROUND
  Recently, increased IL-4 and decreased interferon-gamma (IFN-gamma) production in peripheral blood mononuclear cells (PBMCs) from patients with atopic dermatitis have been reported by several groups. They measured the total amount of each cytokine in culture supernatants in their studies. These studies suggested a predominance of type 2 cytokine-producing cells in atopic dermatitis. However, it is still unclear whether the cytokine imbalance is the result of an imbalance of specific T-cell subsets or of dysregulation of the cytokine-producing ability in T-cell subsets. Here, we examined frequencies of IL-4-, IFN-gamma-, or IL-2-producing CD4+ cells and CD8+ cells in PBMCs from patients with atopic dermatitis at a single cell level by using flow cytometry.
  
  
  METHODS
  PBMCs from 45 patients with atopic dermatitis and 24 healthy control subjects were stimulated with immobilized anti-CD3 monoclonal antibody for 6 hours in the presence of monensin. Cells were fixed, made permeable, and stained for intracellular cytokines in combination with staining for cell surface markers CD4 and CD8.
  
  
  RESULTS
  The frequency of IL-4-producing CD4+ cells and CD8+ cells from patients with atopic dermatitis was significantly higher (p < 0.001) than that from healthy control subjects. In contrast, the frequency of IFN-gamma-producing CD4+ cells and CD8+ cells was significantly decreased (p < 0.01) in the patients with atopic dermatitis. The frequency of IL-2-producing cells from patients with atopic dermatitis was comparable to that from healthy control subjects.
  
  
  CONCLUSIONS
  Our findings indicate that frequencies of type 2 cytokine-producing cells, not only among CD4+ cells but also among CD8+ cells, were significantly higher in patients with atopic dermatitis than in healthy control subjects.
authors.affiliation: Department of Immunology and Parasitology, School of Medicine, Yokohama City University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nakazawa
authors.forename: N
authors.initials: N
authors.lastname: Sugi
authors.forename: H
authors.initials: H
authors.lastname: Kawaguchi
authors.forename: N
authors.initials: N
authors.lastname: Ishii
authors.forename: H
authors.initials: H
authors.lastname: Nakajima
authors.forename: M
authors.initials: M
authors.lastname: Minami
mesh_terms: D000293:Adolescent; D000328:Adult; D017252:CD3 Complex / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism*; D016207:Cytokines / Q000096:biosynthesis*; D003876:Dermatitis, Atopic / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D008297:Male; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000378:metabolism*
chemical_list: D017252:CD3 Complex; D016207:Cytokines; D007376:Interleukin-2; D015847:Interleukin-4; D007371:Interferon-gamma