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Monocytes P2X7 purinergic receptor is modulated by glatiramer acetate in multiple sclerosis

Mariantonietta Caragnano1, Paola Tortorella, Alessandra Bergami

  • 1Department of Medical and Occupational Sci., University of Foggia, Italy.

Journal of Neuroimmunology
|February 29, 2012
PubMed

Insights

Glatiramer Acetate (GA) treatment appears to modulate P2X7 receptor and CD39 expression on monocytes in multiple sclerosis (MS) patients. GA downregulated P2X7 receptor expression in vitro and in vivo, with trends toward altered IL-1beta and CD39 levels.

Area of Science:

  • Immunology
  • Neuroscience
  • Pharmacology

Background:

  • Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system.
  • Monocytes play a role in MS pathogenesis.
  • P2X7 receptor (P2X7R), IL-1beta, and CD39 are involved in immune responses.

Purpose of the Study:

  • To investigate the expression of P2X7R, IL-1beta, and CD39 on monocytes from MS patients.
  • To evaluate the in vitro and in vivo effects of Glatiramer Acetate (GA) on these markers.

Main Methods:

  • Quantitative real-time PCR (qrt-PCR) was used to measure gene expression.
  • Monocytes were isolated from treatment-naïve MS patients and healthy donors (HDs).
  • In vitro GA treatment of stimulated monocytes and in vivo GA treatment of MS patients were assessed.

Main Results:

  • No significant differences in P2X7R, IL-1beta, or CD39 expression were found between MS patients and HDs at baseline.
  • In vitro GA pre-conditioning downregulated P2X7R expression in BzATP-stimulated MS monocytes and HD monocytes.
  • In vivo GA treatment reduced P2X7R and CD39 expression in MS patients after 12 months.

Conclusions:

  • Monocytes from MS patients and healthy individuals express P2X7R, IL-1beta, and CD39.
  • Glatiramer Acetate demonstrates potential to modulate P2X7R, IL-1beta, and CD39 expression on monocytes.
  • These findings suggest a mechanism by which GA may exert its therapeutic effects in MS.

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