Mechanisms of action of glatiramer acetate in multiple sclerosis

Oliver Neuhaus, Cinthia Farina, Hartmut Wekerle, Reinhard Hohlfeld

Research output: Contribution to journalArticle

Abstract

Glatiramer acetate (GA, Copaxone [Teva Pharmaceuticals, Kansas City, MO], formerly known as copolymer-1) and interferon- (IFN)-β are both used for the immunomodulatory treatment of multiple sclerosis, but they act in different ways. Four major mechanisms of GA have been identified: 1) competition with myelin-basic protein (MBP) for binding to major histocompatibility complex (MHC) molecules; 2) competition of GA/MHC with MBP/MHC for binding to the T-cell receptor; 3) partial activation and tolerance induction of MBP-specific T cells (action as an altered peptide ligand); and 4) induction of GA-reactive T-helper 2- (TH2)-like regulatory cells. Of these four mechanisms, 1 and 2 presumably occur only in vitro and are therefore irrelevant for the in vivo effects of GA. In contrast, mechanisms 3 and 4 could occur in vivo and both could contribute to the clinical effects of GA.

Original languageEnglish
Pages (from-to)702-708
Number of pages7
JournalNeurology
Volume56
Issue number6
Publication statusPublished - Mar 27 2001

ASJC Scopus subject areas

  • Neuroscience(all)

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