Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system probably mediated by Th1 lymphocytes. IFN-beta is an established therapy for relapsing MS patients, although the mechanisms underlying its efficacy are yet to be well characterized. We determined IL-2 production, CD25 expression and T-cell proliferation from relapsing-remitting MS patients before and three months after starting therapy. A decrease in the percentage of CD80-induced IL-2-producing cells was observed after in vivo IFN-beta treatment. These data support that one of the immunomodulatory effects of IFN-beta treatment in MS may be a limitation of the autoimmune response modifying the CD80:CD28/CTLA-4 pathway.
Publication types
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Clinical Trial
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Controlled Clinical Trial
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Research Support, Non-U.S. Gov't
MeSH terms
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Adjuvants, Immunologic / administration & dosage*
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Adult
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Animals
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Antigens, CD
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Antigens, Differentiation / metabolism*
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B7-1 Antigen / pharmacology
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CD28 Antigens / metabolism*
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CTLA-4 Antigen
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Cell Division / drug effects
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Cell Division / immunology
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Cell Line, Tumor
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Female
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Humans
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Interferon-beta / administration & dosage*
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Interleukin-2 / metabolism*
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Male
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Mastocytoma
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Middle Aged
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Multiple Sclerosis, Relapsing-Remitting / drug therapy*
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Multiple Sclerosis, Relapsing-Remitting / immunology
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Multiple Sclerosis, Relapsing-Remitting / metabolism
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T-Lymphocytes / cytology
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism
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Up-Regulation / drug effects
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Up-Regulation / immunology
Substances
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Adjuvants, Immunologic
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Antigens, CD
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Antigens, Differentiation
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B7-1 Antigen
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CD28 Antigens
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CTLA-4 Antigen
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CTLA4 protein, human
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Interleukin-2
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Interferon-beta