Abstract
Interferon (IFN)-beta, the most effective immunomodulatory treatment for MS, inhibits the proliferation of myelin-specific T cells. We report that IFN-beta moderately enhances the expression of the death receptor, CD95, at the surface of human antigen-specific T cells. However, T-cell apoptosis was not induced by IFNbeta-1a or IFNbeta-1b as assessed by caspase activity or DNA fragmentation. Immunomodulation mediated by IFN-beta does not directly involve apoptotic pathways in human T cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adjuvants, Immunologic / pharmacology*
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Apoptosis / drug effects*
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Apoptosis / immunology*
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Caspase 3
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Caspases / immunology
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Caspases / metabolism
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Coumarins / metabolism
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Coumarins / pharmacology
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DNA Fragmentation
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Epitopes
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Fluorescent Dyes / metabolism
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Fluorescent Dyes / pharmacology
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Gene Expression / immunology
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Humans
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In Vitro Techniques
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Interferon-beta / pharmacology*
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Multiple Sclerosis / immunology*
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Myelin Basic Protein / immunology
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Oligopeptides / metabolism
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Oligopeptides / pharmacology
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RNA, Messenger / analysis
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T-Lymphocytes / enzymology
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T-Lymphocytes / immunology*
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fas Receptor / genetics
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fas Receptor / immunology
Substances
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Adjuvants, Immunologic
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Coumarins
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Epitopes
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Fluorescent Dyes
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Myelin Basic Protein
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Oligopeptides
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RNA, Messenger
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acetyl-aspartyl-glutamyl-valyl-aspartyl-amino-4-methylcoumarin
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fas Receptor
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Interferon-beta
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CASP3 protein, human
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Caspase 3
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Caspases