Interferon beta1a treatment modulates TH1 expression in gammadelta + T cells from relapsing-remitting multiple sclerosis patients

Abstract

A paradigm exists that multiple sclerosis is causally related to dysregulation of TH1 inflammatory cytokines and TH2 antiinflammatory cytokines. The cytokine source(s) that initiate the imbalances are unknown. In this study, gammadelta, 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 beta-1a (IFNbeta1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon gamma (IFNgamma), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFN-gamma, IL10, and IL12 from each cell type did not change significantly with IFNbeta1a treatment. The IL10 secreted by gammadelta TCR+ cells strongly correlated with the IL12 secreted by the same gammadelta TCR+ cells, supporting the paradigm. Furthermore, IFNbeta1a therapy decreased the gammadelta TCR+ cell secretion of TH1 cytokines after 8-10 weeks of therapy.