Intracellular cytokine patterns in Behçet’s disease in comparison to ankylosing spondylitis – influence of treatment with interferon-α2a

M. Amberger, S. Groll, I. Günaydin, C. Deuter, R. Vonthein, I. Kötter

1University Hospital, Department of Internal Medicine II, Otfried-Mueller-Str. 10, D-72076 Tübingen, Germany.

2007 Vol.25, N°4 ,Suppl.45 - PI 0052, PF 0057
Full Paper

Rheumatology Article



Treatment of Behçet’s disease (BD) with human recombinant interferon-α2a (IFN-α2a) has proven clinically effective. The mechanism of action is unknown. This is the first study investigating the influence of IFN-α2a on intracellular cytokines in T-cells in patients with BD in comparison to healthy controls and to patients with ankylosing spondylitis (AS).
Cytokine expression of T-cells was investigated in 10 patients with BD before and 4 and 12 weeks after initiation of treatment with IFN-α2a. 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-α (TNF-α), interferon-&ggr; (IFN-&ggr;) and interleukin 4 (IL 4).
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-α2a treatment (p < 0.001). CD4+ T-cells producing IFN-&ggr; and TNF-α increased significantly (p = 0.002 and p = 0.01). CONLUSION: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-α2a induces restoration of IL 2-production in patients with BD which is likely to be one mechanism of action of IFN-α2a.

PMID: 17949552 [PubMed]