Disease-modifying treatments modulate myeloid cells in multiple sclerosis patients

Neurol Sci. 2018 Feb;39(2):373-376. doi: 10.1007/s10072-017-3176-2. Epub 2017 Nov 28.

Abstract

The role of myeloid cells in the pathogenesis of MS is determined by the polarization they acquire after activation, and mediated by release of extracellular vesicles (MVs). We assessed the effects of treatments for MS on activation and polarization of myeloid cells. MVs levels and markers of polarization of myeloid cells have been assessed at baseline and up to 6 months after the start of a MS treatment. Patients had higher levels of MVs than controls, and these increased significantly over 6 months under natalizumab. Interferon β-1a significantly decreased M1 pro-inflammatory marker IL1β and upregulated Trem2, a receptor important for debris clearance; both interferon β-1a and fingolimod decreased pro-inflammatory marker IL6. Current treatments for MS significantly modulate myeloid cells activity.

Keywords: Disease modifying drugs; Extracellular vesicles; Interleukin-1β; Multiple sclerosis; Myeloid cells; Trem2.

MeSH terms

  • Adult
  • Case-Control Studies
  • Cell Polarity / drug effects
  • Cohort Studies
  • Extracellular Vesicles
  • Female
  • Fingolimod Hydrochloride / therapeutic use
  • Humans
  • Immunologic Factors / therapeutic use*
  • Interferon beta-1a / therapeutic use
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Male
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism
  • Middle Aged
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / pathology*
  • Myeloid Cells / drug effects*
  • Myeloid Cells / pathology
  • Natalizumab / therapeutic use
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / metabolism
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Time Factors

Substances

  • IL1B protein, human
  • Immunologic Factors
  • Interleukin-1beta
  • Membrane Glycoproteins
  • Natalizumab
  • Receptors, Immunologic
  • TREM2 protein, human
  • Superoxide Dismutase
  • superoxide dismutase 2
  • Fingolimod Hydrochloride
  • Interferon beta-1a