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

J Neuroimmunol. 2009 Oct 30;215(1-2):125-8. doi: 10.1016/j.jneuroim.2009.08.007. Epub 2009 Sep 15.

Abstract

Disease modifying effects of interferon (IFN)-beta therapy in patients with multiple sclerosis (MS) may be mediated in part through enhanced immunoregulation by the CD56(bright) subpopulation of natural killer (NK) cells and by Foxp3+ (not italicized) CD4+CD25+ regulatory T cells (Treg). We found that IFN-beta-1a(IM) treatment of relapsing-remitting (RR)MS subjects over 12 months significantly increased both percentage of CD56(bright) 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-beta-1a in MS include control of pernicious autoimmunity.

Publication types

  • Clinical Trial, Phase IV
  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adult
  • CD56 Antigen / biosynthesis*
  • Female
  • Forkhead Transcription Factors / biosynthesis*
  • Forkhead Transcription Factors / genetics
  • Humans
  • Interferon beta-1a
  • Interferon-beta / therapeutic use*
  • Killer Cells, Natural / immunology*
  • Killer Cells, Natural / metabolism
  • Killer Cells, Natural / pathology
  • Lymphocyte Count
  • Male
  • Middle Aged
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / pathology
  • Multiple Sclerosis / therapy
  • Pilot Projects
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • Treatment Outcome
  • Up-Regulation / immunology*
  • Young Adult

Substances

  • CD56 Antigen
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Interferon-beta
  • Interferon beta-1a