title: Reduced IFN-γ receptor expression and attenuated IFN-γ response by dendritic cells in patients with atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is characterized by a predominance of T(H)2 immune reactions but weaker T(H)1 immune responses in acute skin lesions.
  
  
  OBJECTIVE
  To evaluate whether enhanced T(H)2 immunity in patients with AD might impair T(H)1 immune responses by affecting the IFN-γ responsiveness of antigen-presenting cells, we investigated IFN-γ receptor and IL-4 receptor α chain expression, IFN-γ signaling, and the expression of IFN-γ-responsive mediators in dendritic cells (DCs) and their precursors from patients with AD compared with those from healthy subjects.
  
  
  METHODS
  Skin biopsy specimens were obtained and both monocytes and monocyte-derived dendritic cells (MoDCs) from patients with AD (n = 86) and control subjects (n = 84) were analyzed by means of flow cytometry, real-time PCR, ELISA, and HPLC.
  
  
  RESULTS
  We observed lower IFN-γ receptor II expression combined with higher IL-4 receptor α chain expression on epidermal DCs, monocytes, and MoDCs from patients with AD. Induction of IFN-γ-inducible factors, such as interferon regulatory factor 1, interferon-inducible protein 10, and indoleamine 2,3-dioxygenase, was attenuated in IFN-γ-pulsed MoDCs from patients with AD. Weaker signal transducer and activator of transcription 1 activation mirrored by lower phosphorylated signal transducer and activator of transcription 1 levels in response to IFN-γ stimulation could be observed in epidermal DCs, monocytes, and MoDCs from patients with AD.
  
  
  CONCLUSIONS
  Impaired IFN-γ signaling together with attenuated IFN-γ responses in DCs and their precursor cells might contribute to the T(H)2 bias in patients with AD.
authors.affiliation: Department of Dermatology and Allergy, University of Bonn Medical Center, Bonn, Germany.
authors.forename: Eva
authors.initials: E
authors.lastname: Gros
authors.forename: Susanne
authors.initials: S
authors.lastname: Petzold
authors.forename: Laura
authors.initials: L
authors.lastname: Maintz
authors.forename: Thomas
authors.initials: T
authors.lastname: Bieber
authors.forename: Natalija
authors.initials: N
authors.lastname: Novak
mesh_terms: D000328:Adult; D002469:Cell Separation; D002851:Chromatography, High Pressure Liquid; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism*; D008297:Male; D060888:Real-Time Polymerase Chain Reaction; D017471:Receptors, Interferon / Q000096:biosynthesis* / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism; D000096743:Interferon gamma Receptor
chemical_list: D007371:Interferon-gamma; D017471:Receptors, Interferon; D000096743:Interferon gamma Receptor