文摘
A paradigm exists that multiple sclerosis is causally related to dysregulation of T1 inflammatory cytokines and T2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, &ggr;&dgr;, CD4, and CD8 T cell receptor-positive (TCR+) cells were isolated from the blood of 26 definitive relapsing-remitting multiple sclerosis patients prior to interferon &bgr;-1a (IFN&bgr;1a) therapy and following 8–10 weeks of this therapy. The bioactivities of interferon &ggr; (IFN&ggr;), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFN&ggr;, IL10, and IL12 from each cell type did not change significantly with IFN&bgr;1a treatment. The IL10 secreted by &ggr;&dgr; TCR+ cells strongly correlated with the IL12 secreted by the same &ggr;&dgr; TCR+ cells, supporting the paradigm. Furthermore, IFN&bgr;1a therapy decreased the &ggr;&dgr; TCR+ cell secretion of T1 cytokines after 8–10 weeks of therapy.