title: Intracellular cytokine patterns in Behçet's disease in comparison to ankylosing spondylitis--influence of treatment with interferon-alpha2a.
abstract: OBJECTIVE
  Treatment of Behçet's disease (BD) with human recombinant interferon-alpha2a (IFN-alpha2a) has proven clinically effective. The mechanism of action is unknown. This is the first study investigating the influence of IFN-alpha2a on intracellular cytokines in T-cells in patients with BD in comparison to healthy controls and to patients with ankylosing spondylitis (AS).
  
  
  METHODS
  Cytokine expression of T-cells was investigated in 10 patients with BD before and 4 and 12 weeks after initiation of treatment with IFN-alpha2a. 10 patients with AS and 10 healthy individuals served as controls. Peripheral blood mononuclear cells were assayed by flow cytometry for the cell surface markers CD3, CD8 and CD4 and for the intracellular cytokines interleukin 2 (IL 2), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin 4 (IL 4).
  
  
  RESULTS
  The fraction of CD3+ and CD4+ T-cells producing IL 2 was significantly lower in untreated BD and AS patients compared to healthy controls (p = 0.02 and 0.007). However, the number of IFN-g-producing CD3+ T-cells in untreated BD patients was elevated in comparison to both control groups (p = 0.05). T-cell cytokine analysis of BD patients revealed a significant increase of IL 2-production in T-cells during IFN-alpha2a treatment (p < 0.001). CD4+ T-cells producing IFN-gamma and TNF-alpha increased significantly (p = 0.002 and p = 0.01).
  
  
  CONCLUSIONS
  In BD and AS, CD3+ and CD4+ T-cells producing IL 2 are reduced. This may hint at a similarity in the pathogenesis of these HLA-class I-associated disorders. IFN-alpha2a induces restoration of IL 2-production in patients with BD which is likely to be one mechanism of action of IFN-alpha2a.
authors.affiliation: University Hospital, Department of Internal Medicine II, Otfried-Mueller-Str. 10, D-72076 Tübingen, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Amberger
authors.forename: S
authors.initials: S
authors.lastname: Groll
authors.forename: I
authors.initials: I
authors.lastname: Günaydin
authors.forename: C
authors.initials: C
authors.lastname: Deuter
authors.forename: R
authors.initials: R
authors.lastname: Vonthein
authors.forename: I
authors.initials: I
authors.lastname: Kötter
mesh_terms: D000328:Adult; D001528:Behcet Syndrome / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D017252:CD3 Complex / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology*; D007371:Interferon-gamma / Q000187:drug effects; D007376:Interleukin-2 / Q000378:metabolism; D008297:Male; D011994:Recombinant Proteins; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects
chemical_list: D017252:CD3 Complex; D007155:Immunologic Factors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D007376:Interleukin-2; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma