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From the Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
M. Pette is a research fellow of the Deutsche Forschungsgemeinschaft (Pe 363/7-1). P. Muraro is supported by the Italian MS Society. R. Martin is a Heisenberg fellow of the Deutsche Forschungsgemeinschaft (Ma 965/4-1).
Address correspondence and reprint requests to Dr. Martin Pette, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 5B16, 10 Center Drive MSC 1400, Bethesda, MD 20892-1400.
Interferon-ß (IFN-ß) 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-
(IFN-) and/or tumor necrosis factor-
(TNF-). In this study we investigated the the effects of human recombinant IFN-ß1b on proliferation, interleukin 2 (IL-2) receptor (IL-2R) -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-ß partially suppressed both antigen- and IL-2-driven proliferation of these cells without affecting the expression of either IL-2 or IL-2R-chain. There was no inhibitory effect on the secretion of IFN-, TNF-, and macrophage inflammatory protein (MIP)-1, but release was rather slightly enhanced. In conclusion, while IFN-ß 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-ß on MS may not depend on a primary inhibition of potentially encephalitogenic T lymphocytes.
Received December 5, 1996. Accepted in final form February 19, 1997.
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