title: Cyclosporine in atopic dermatitis. Modulation in the expression of immunologic markers in lesional skin.
abstract: BACKGROUND
  In previous studies, oral cyclosporine was highly effective in the treatment of patients with severe atopic dermatitis. In this study seven patients with severe and therapy-resistant atopic dermatitis underwent therapy with cyclosporine, 5 mg/kg/day, for 6 weeks.
  
  
  OBJECTIVE
  The effect of cyclosporine on the expression of cytokines, which probably play a role in this disease, was examined.
  
  
  METHODS
  The study was performed with a panel of antibodies as markers of inflammatory cells, adhesion molecules, and cytokines (interferon-gamma [IFN-gamma], tumor necrosis factor-alpha [TNF-alpha] and interleukins 1 alpha, 1 beta, and 8 [IL-1 alpha, IL-1 beta, and IL-8, respectively]). They were visualized by indirect immunoperoxidase techniques.
  
  
  RESULTS
  After 2 weeks of cyclosporine therapy, a reduction of 60% in the disease (severity and extent) was observed. This reduction was 89% after 4 weeks and 90% after 6 weeks of therapy. Results of indirect immunoperoxidase stains performed on lesional skin sections after 2 weeks of treatment showed statistically significant reduced numbers of CD14+, CD25 (IL-2R+) and IL-8+ inflammatory cells in the dermis and CD36(OKM5)+ cells in both the epidermis and dermis. The number of cells expressing IFN-gamma and TNF-alpha, assumed to be the products of the helper T-cell (TH)1 subset, was unaltered despite the impressive clinical benefit observed. Keratinocytes in lesional atopic skin did not express intercellular adhesion molecule type 1 (ICAM-1). The expression of the adhesion molecules ICAM-1, lymphocyte function-associated (LFA) type 1, and LFA-3 on inflammatory cells also remained unaffected by cyclosporine treatment.
  
  
  CONCLUSIONS
  A statistically significant reduction in the number of activated T cells and in the number of cells expressing the IL-2 receptor (CD25) paralleled a marked improvement in the disease and supports the view that atopic dermatitis is based on a T-cell-mediated immune inflammation.
authors: Department of Dermato-Venereology, Erasmus University, Rotterdam, The Netherlands.
authors: T
authors: T
authors: van Joost
authors: M M
authors: MM
authors: Kozel
authors: B
authors: B
authors: Tank
authors: R
authors: R
authors: Troost
authors: E P
authors: EP
authors: Prens
mesh_terms: D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D000943:Antigens, Differentiation / Q000032:analysis*; D015415:Biomarkers / Q000032:analysis; D016572:Cyclosporine / Q000627:therapeutic use*; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D008297:Male; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000943:Antigens, Differentiation; D015415:Biomarkers; D015375:Receptors, Interleukin-2; D016572:Cyclosporine