Recent insights into the mechanism of action of glatiramer acetate

J Neuroimmunol. 2011 Jun;235(1-2):9-17. doi: 10.1016/j.jneuroim.2011.01.009. Epub 2011 Mar 13.

Abstract

Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology
  • Dendritic Cells / drug effects
  • Dendritic Cells / immunology
  • Dendritic Cells / pathology
  • Glatiramer Acetate
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Immunosuppressive Agents / therapeutic use*
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / pathology
  • Peptides / pharmacology
  • Peptides / therapeutic use*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / pathology

Substances

  • Immunosuppressive Agents
  • Peptides
  • Glatiramer Acetate