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Invest. Ophthalmol. Vis. Sci. · May 1998
Increased frequencies of interleukin-2- and interferon-gamma-producing T cells in patients with active Behçet's disease.
- N Sugi-Ikai, M Nakazawa, S Nakamura, S Ohno, and M Minami.
- Department of Ophthalmology, Yokohama City University School of Medicine, Yokohama, Japan.
- Invest. Ophthalmol. Vis. Sci. 1998 May 1; 39 (6): 996-1004.
PurposeTo elucidate the profile of cytokine-producing T cells in patients with active or inactive Behçet's disease (BD), the frequencies of type 1 (Interleukin- [IL] 2, interferon-gamma [IFN-gamma]) and type 2 (IL-4) cytokine-producing CD4+ and CD8+ cells in peripheral blood were investigated, and the effect of immunosuppressive drugs on the profile of cytokine-producing cells was evaluated.MethodsFifty-two patients with BD (32 with active and 20 with inactive BD) and 33 healthy control subjects were the subjects in this study. Patients were or were not treated with immunosuppressive drugs. Peripheral blood mononuclear cells were fixed, permeabilized, and stained for intracellular cytokines in combination with cell surface markers CD4 and CD8 for flow cytometric analysis.ResultsIn nontreated patients with BD, the frequencies of IL-2- and IFN-gamma-producing CD4 and CD8+ cells in active patients were significantly higher than those in inactive patients. Conversely, the frequencies of IL-4 producing CD4+ and CD8+ cells in nontreated patients with active BD were comparable with those in patients with inactive disease and in control subjects. Patients with inactive BD who were treated with immunosuppressive drugs showed significantly lower frequencies of IL-2- and IFN-gamma-producing CD4+ and CD8+ cells than did treated patients with active BD.ConclusionsThe frequencies of type 1 cytokine-producing CD4+ and CD8+ cells increased in patients with active BD. Effective immunosuppressive treatments decreased the population of type 1 cytokine-producing CD4+ and CD8+ cells. These results suggest that type 1 cytokine-producing cells play an important role in the immunopathogenesis of the inflammation in BD.
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