title: FcepsilonRI engagement of Langerhans cell-like dendritic cells and inflammatory dendritic epidermal cell-like dendritic cells induces chemotactic signals and different T-cell phenotypes in vitro.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a biphasic inflammatory skin disease characterized by an initial phase predominated by T(H)2 cytokines, which switches into a second T(H)1-dominated chronic phase. Thus far, the small number of FcepsilonRI-bearing Langerhans cells (LCs) and inflammatory dendritic epidermal cells (IDECs) in the epidermis of patients with AD has hampered a detailed functional analysis and limited our knowledge of these dendritic cells (DCs).
  
  
  OBJECTIVE
  We studied FcepsilonRI-mediated mechanisms of LCs and IDECs with the help of a novel in vitro model.
  
  
  METHODS
  Langerhans cell-like dendritic cells (LC-DCs) and inflammatory dendritic epidermal cell-like dendritic cells (IDEC-DCs) bearing FcepsilonRI have been generated from monocytes of the same atopic donor and compared functionally with LCs and IDECs isolated from the skin of patients with AD.
  
  
  RESULTS
  We found that FcepsilonRI-activated LC-DCs release chemotactic signals, and supernatants of FcepsilonRI-activated LC-DCs increase the migratory capacity of precursor cells of IDECs and naive T cells in vitro. FcepsilonRI-activated IDEC-DCs produce high amounts of proinflammatory cytokines and chemokines and might thereby amplify the inflammatory immune reaction in patients with AD. Furthermore, FcepsilonRI-activated IDEC-DCs prime naive T cells into IFN-gamma-producing T cells and release IL-12 and IL-18, which together might lead to the switch of the initial T(H)2-type immune response into a response of the T(H)1 type in vivo.
  
  
  CONCLUSIONS
  The present study provides evidence that FcepsilonRI-activated LC-DCs and IDEC-DCs contribute distinctly to the outcome of T-cell responses in vitro and might have implications for the biphasic nature of AD in vivo.
authors.affiliation: Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany.
authors.forename: Natalija
authors.initials: N
authors.lastname: Novak
authors.forename: Rudolf
authors.initials: R
authors.lastname: Valenta
authors.forename: Barbara
authors.initials: B
authors.lastname: Bohle
authors.forename: Sylvia
authors.initials: S
authors.lastname: Laffer
authors.forename: Jörg
authors.initials: J
authors.lastname: Haberstok
authors.forename: Stefan
authors.initials: S
authors.lastname: Kraft
authors.forename: Thomas
authors.initials: T
authors.lastname: Bieber
mesh_terms: D017951:Antigen Presentation; D018925:Chemokines / Q000096:biosynthesis; D002630:Chemotactic Factors / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D004817:Epidermis / Q000276:immunology; D006801:Humans; D066298:In Vitro Techniques; D007801:Langerhans Cells / Q000276:immunology; D008213:Lymphocyte Activation; D009000:Monocytes / Q000276:immunology; D010641:Phenotype; D017455:Receptors, IgE / Q000378:metabolism*; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D018925:Chemokines; D002630:Chemotactic Factors; D016207:Cytokines; D017455:Receptors, IgE