Interferon β1a treatment modulates TH1 expression in γδ + T cells from relapsing-remitting multiple sclerosis patients

Cerise L. Elliott, Samia Y. Ei-Touny, Mary L. Filipi, Kathleen M. Healey, M. Patricia Leuschen

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


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, γδ, 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 β-1a (IFNβ1a) therapy and following 8-10 weeks of this therapy. The bioactivities of interferon γ (IFNγ), interleukin 10 (IL10), and interleukin 12 (IL12) were determined. The concentrations of IFNγ, IL10, and IL12 from each cell type did not change significantly with IFNβ1a treatment. The IL10 secreted by γδ TCR+ cells strongly correlated with the IL12 secreted by the same γδ TCR+ cells, supporting the paradigm. Furthermore, IFNβ1a therapy decreased the γδ TCR+ cell secretion of TH1 cytokines after 8-10 weeks of therapy.

Original languageEnglish (US)
Pages (from-to)200-209
Number of pages10
JournalJournal of Clinical Immunology
Issue number3
StatePublished - 2001


  • Interferon β1a interleukin 12
  • Interleukin 10
  • Multiple sclerosis
  • γδ T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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