Interferon beta 1a treatment modulates T(H)1 expression in gamma delta plus T cells from relapsing-remitting multiple sclerosis patients

A paradigm exists that multiple sclerosis is causally related to dysregulat ion of T(H)1 inflammatory cytokines and T(H)2 antiinflammatory cytokines. T he cytokine source(s) that initiate the imbalances are unknown. In this stu dy, gamma delta, CD4, and CD8 T cell receptor-positive (TCR+) cells were is olated from the blood of 26 definitive relapsing-remitting multiple scleros is patients prior to interferon beta -1a (IFN beta 1a) therapy and followin g 8-10 weeks of this therapy. The bioactivities of interferon gamma (IFN ga mma), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFN gamma, IL10, and IL12 from each cell type did not ch ange significantly with IFN beta 1a treatment. The IL10 secreted by ya TCR cells strongly correlated with the IL12 secreted by the same ya TCR+ cells , supporting the paradigm. Furthermore, IFN beta 1a therapy decreased the g amma delta TCR+ cell secretion of T(H)1 cytokines after 8-10 weeks of thera py.