Interferon-β (IFN-β) has beneficial effects on the frequency and severity of relapses, as well as on disease progression in patients suffering from relapsing-remitting MS. Its mode of action, however, is not completely understood. Previous studies on T-lymphocyte bulk cultures and T-lymphocyte lines with specificity for different antigens suggested that the drug might partially act via suppression of T-cell proliferation and secretion of proinflammatory cytokines like interferon-γ (IFN-γ) and/or tumor necrosis factor-α (TNF-α). In this study we investigated the effects of human recombinant IFN-β(1b) on proliferation, interleukin 2 (IL-2) receptor (IL- 2R) α-chain upregulation, and cytokine and chemokine secretion of myelin basic protein-reactive, MS patient-derived T-cell clones secreting T-helper type 1 (Th1) cytokines. IFN-β partially suppressed both antigen- and IL-2- driven proliferation of these cells without affecting the expression of either IL-2 or IL-2R α-chain. There was no inhibitory effect on the secretion of IFN-γ, TNF-α, and macrophage inflammatory protein (MIP)-1α, but release was rather slightly enhanced. In conclusion, while IFN-β does reduce proliferation of Th1-like, MBP-specific T cells in vitro, the drug does not result in overall dysfunction of these cells. Therefore, the effect of IFN-β on MS may not depend on a primary inhibition of potentially encephalitogenic T lymphocytes.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Aug 1997|
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