Interferon-beta-1a treatment increases CD56bright natural killer cells and CD4+CD25+ Foxp3 expression in subjects with multiple sclerosis

Arthur A. Vandenbark, Jianya Huan, Marisa Agotsch, Dorian La Tocha, Susan Goelz, Halina Offner, Stefan Lanker, Dennis Bourdette

Research output: Contribution to journalArticle

73 Scopus citations

Abstract

Disease modifying effects of interferon (IFN)-β therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56bright subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-β-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56bright NK cells and Foxp3 mRNA expression compared to baseline values, untreated RRMS subjects and healthy controls (HC). This striking enhancement of two prominent immunoregulatory pathways lends support to the idea that beneficial effects of IFN-β-1a in MS include control of pernicious autoimmunity.

Original languageEnglish (US)
Pages (from-to)125-128
Number of pages4
JournalJournal of Neuroimmunology
Volume215
Issue number1-2
DOIs
StatePublished - Oct 30 2009

Keywords

  • CD56 NK cells
  • Foxp3 expression
  • IFN-β-1a
  • Multiple sclerosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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