title: Expansion of FOXP3-positive CD4+CD25+ T cells associated with disease activity in atopic dermatitis.
abstract: BACKGROUND
  FOXP3-positive CD4+CD25+ T cells are known to have an immunoregulatory function by means of preventing T-cell reactivity to both self- and non-self-antigens. However, the role of these cells in the pathogenesis of allergic diseases is not clear.
  
  
  OBJECTIVE
  To evaluate the quantity and quality of circulating FOXP3-positive T cells in patients with atopic dermatitis (AD).
  
  
  METHODS
  Peripheral blood mononuclear cells were isolated from 35 AD patients (mean [SD] age, 27.1 [7.5] years) and 36 controls (mean [SD] age, 27.5 [10.0] years). Cellular FOXP3 expression was analyzed using flow cytometry. Characteristics of FOXP3-positive T cells were evaluated with respect to cytokine production capability and suppressive function.
  
  
  RESULTS
  Frequencies of circulating FOXP3+CD25+ cells in the CD4+ T-cell population of AD patients were significantly higher than those in controls (mean [SD], 7.4% [4.6%] vs 4.5% [1.3%]; P = .002) and correlated with their Scoring Atopic Dermatitis (SCORAD) scores (r = 0.74, P = .008) and peripheral blood eosinophil counts (r = 0.72, P < .001). In the patients whose samples were analyzed at intervals of 1 to 2 months, frequencies of FOXP3-positive T cells were decreased as their skin lesions improved, regardless of medicines used. FOXP3-positive CD4+ T cells from patients, as well as those from controls, showed little capability to synthesize interferon gamma and interleukin 4. No differences were found in suppression abilities of CD4+CD25+ T cells between AD patients and controls.
  
  
  CONCLUSIONS
  Our data suggest that dynamic fluctuation in numbers of circulating FOXP3-positive regulatory T cells might contribute to the pathogenesis of AD.
authors.affiliation: Department of Pediatrics, Graduate School of Medicine, University of Toyama, Toyama, Japan.
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Ito
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Adachi
authors.forename: Teruhiko
authors.initials: T
authors.lastname: Makino
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Higashiyama
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Fuchizawa
authors.forename: Tadamichi
authors.initials: T
authors.lastname: Shimizu
authors.forename: Toshio
authors.initials: T
authors.lastname: Miyawaki
mesh_terms: D000293:Adolescent; D000328:Adult; D018791:CD4 Lymphocyte Count; D018920:Coculture Techniques; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000276:immunology*; D004804:Eosinophils / Q000166:cytology; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism*; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism*; D015847:Interleukin-4 / Q000378:metabolism; D007958:Leukocyte Count; D008297:Male; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D055815:Young Adult
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508017:IL2RA protein, human; C508598:IL4 protein, human; D053645:Interleukin-2 Receptor alpha Subunit; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma