The Evolving Mechanisms of Action of Glatiramer Acetate

Cold Spring Harb Perspect Med. 2019 Feb 1;9(2):a029249. doi: 10.1101/cshperspect.a029249.


Glatiramer acetate (GA) is a synthetic amino acid copolymer that is approved for treatment of relapsing remitting multiple sclerosis (RRMS) and clinically isolated syndrome (CIS). GA reduces multiple sclerosis (MS) disease activity and has shown comparable efficacy with high-dose interferon-β. The mechanism of action (MOA) of GA has long been an enigma. Originally, it was recognized that GA treatment promoted expansion of GA-reactive T-helper 2 and regulatory T cells, and induced the release of neurotrophic factors. However, GA treatment influences both innate and adaptive immune compartments, and it is now recognized that antigen-presenting cells (APCs) are the initial cellular targets for GA. The anti-inflammatory (M2) APCs induced following treatment with GA are responsible for the induction of anti-inflammatory T cells that contribute to its therapeutic benefit. Here, we review studies that have shaped our current understanding of the MOA of GA.

Publication types

  • Review

MeSH terms

  • Animals
  • Glatiramer Acetate / immunology
  • Glatiramer Acetate / therapeutic use*
  • Humans
  • Immunosuppressive Agents / immunology
  • Immunosuppressive Agents / therapeutic use*
  • Mice
  • Multiple Sclerosis / drug therapy
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Multiple Sclerosis, Relapsing-Remitting / immunology
  • Randomized Controlled Trials as Topic


  • Immunosuppressive Agents
  • Glatiramer Acetate