Interferon beta-1a therapy enhances CD4+ regulatory T-cell function: an ex vivo and in vitro longitudinal study in relapsing-remitting multiple sclerosis

J Neuroimmunol. 2007 Jan;182(1-2):204-11. doi: 10.1016/j.jneuroim.2006.09.012. Epub 2006 Dec 8.

Abstract

Interferon beta-1a (IFNâ-1a) has demonstrated efficacy in multiple sclerosis (MS), although its mechanism of action remains only partly understood. We evaluated the ex vivo and in vitro effects of IFNâ-1a (Rebif) on regulatory T-cell (T(Reg)) function in 22 relapsing-remitting MS patients and 16 healthy controls. T(Reg) function was significantly enhanced after 3 and 6 months of IFNbeta-1a therapy. Furthermore, there was a trend towards increasing proportions of total CD4(+)CD25(+) and CD4(+)CD25(+)GITR(+) T(Reg) after 6 months of IFNbeta-1a therapy when compared with baseline. In conclusion, IFNbeta-1a therapy enhances T(Reg) function, and this may be relevant in the inflammatory environment of MS lesions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adjuvants, Immunologic / therapeutic use*
  • Adult
  • CD4-Positive T-Lymphocytes / metabolism
  • Cohort Studies
  • Female
  • Glucocorticoid-Induced TNFR-Related Protein
  • Humans
  • In Vitro Techniques
  • Interferon beta-1a
  • Interferon-beta / therapeutic use*
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Longitudinal Studies
  • Male
  • Middle Aged
  • Multiple Sclerosis, Relapsing-Remitting / blood
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Multiple Sclerosis, Relapsing-Remitting / immunology*
  • Multiple Sclerosis, Relapsing-Remitting / metabolism
  • Receptors, Nerve Growth Factor / metabolism
  • Receptors, Tumor Necrosis Factor / metabolism
  • T-Lymphocyte Subsets / pathology
  • T-Lymphocytes, Regulatory / immunology*
  • Treatment Outcome

Substances

  • Adjuvants, Immunologic
  • Glucocorticoid-Induced TNFR-Related Protein
  • Interleukin-2 Receptor alpha Subunit
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • TNFRSF18 protein, human
  • Interferon-beta
  • Interferon beta-1a