title: Impaired interferon-gamma production in a subset population of severe atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritic chronic eczema. The immunopathogenesis of this condition is still not well understood. We assessed the transcription and production of IFN-gamma, the Th1 cytokine, and the Th2 cytokine IL-5 in peripheral blood mononuclear cells (PBMCs) from patients with severe AD.
  
  
  METHODS
  The subjects included 17 severe (serum IgE: 5,000-92,000 U/ml, median: 20,000 U/ml), 4 mild AD (IgE: 2-520 U/ml) and 8 nonatopic controls (IgE: <100 U/ml). The severe AD patients were classified into two groups according to the response to standard treatment with topical glucocorticoids. Individuals were classified as poorly responsive (AD-P) if the clinical score decreased less than one third after 2 weeks of hospital treatment and as responsive (AD-R) if the score decreased more than one third. PBMCs isolated from the subjects were stimulated with PHA and PMA.
  
  
  RESULTS
  The expression of IFN-gamma in PBMCs in the AD-P group was much lower than that observed in the other groups at both mRNA and protein levels. There were no significant differences in the levels of IL-5 both in mRNA and protein levels between the groups. There were no significant differences in STAT4 DNA-binding activity following PHA/IL-2/IL-12 stimulation between AD-P and controls.
  
  
  CONCLUSIONS
  These results suggest that the decreased INF-gamma production may account for the abnormal immunopathogenesis of severe, intractable AD.
authors.affiliation: Department of Pediatrics, Jikei University School of Medicine, National Children's Research Center, Tokyo, Japan. tkatsunuma@jikei.ac.jp
authors.forename: Toshio
authors.initials: T
authors.lastname: Katsunuma
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Kawahara
authors.forename: Keisuke
authors.initials: K
authors.lastname: Yuki
authors.forename: Akira
authors.initials: A
authors.lastname: Akasawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Saito
mesh_terms: D000293:Adolescent; D000328:Adult; D017252:CD3 Complex / Q000378:metabolism; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D004268:DNA-Binding Proteins / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology*; D024202:Electrophoretic Mobility Shift Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis*; D015848:Interleukin-5 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D018123:Receptors, Interleukin / Q000096:biosynthesis; D053707:Receptors, Interleukin-12; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050797:STAT4 Transcription Factor; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D015534:Trans-Activators / Q000378:metabolism
chemical_list: D017252:CD3 Complex; D004268:DNA-Binding Proteins; D015848:Interleukin-5; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053707:Receptors, Interleukin-12; D050797:STAT4 Transcription Factor; C494090:STAT4 protein, human; D015534:Trans-Activators; D007371:Interferon-gamma