The Evolving Mechanisms of Action of Glatiramer Acetate.

Abstract

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.

• Authors: Thomas Prod'homme, Scott S Zamvil
• Journal: Cold Spring Harbor perspectives in medicine (Cold Spring Harb Perspect Med) Vol. 9 Issue 2 (02 01 2019) ISSN: 2157-1422 [Electronic] United States
• PMID: 29440323 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2019 Cold Spring Harbor Laboratory Press; all rights reserved.

Chemical References

• Immunosuppressive Agents
• Glatiramer Acetate

Topics

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