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.
IFN-beta treatment modulates the CD28/CTLA-4-mediated pathway for IL-2 production in patients with relapsing-remitting multiple sclerosis. Mult Scler. 2004,10:630-5 / Espoejo, C; Brieva, L; Ruggiero, Giuseppina; Rio, J; Montalban, X; MARTINEZ CACERES, Em. - In: MULTIPLE SCLEROSIS. - ISSN 1352-4585. - STAMPA. - 10:(2004), pp. 630-635.
IFN-beta treatment modulates the CD28/CTLA-4-mediated pathway for IL-2 production in patients with relapsing-remitting multiple sclerosis. Mult Scler. 2004,10:630-5.
RUGGIERO, GIUSEPPINA;
2004
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.| File | Dimensione | Formato | |
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