Probing into the realm of proteins and immunity

Sela, Michael

doi:10.1002/pro.5560070723

Cited by 5 publications

(1 citation statement)

References 28 publications

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“…17,18 Daily s.c. administration of GA has beneficial effects on the clinical and MRI-defined course of patients with MS. [19][20][21][22][23][24] Overview of the immunologic effects of GA in EAE. During the last three decades, the pioneering work of Michael Sela, Ruth Arnon, and their colleagues has laid the foundations for the approval of GA for use in the treatment of MS. 6,25 A large body of experimental evidence in numerous EAE models suggests that GA acts by several different mechanisms 7 :…”

mentioning

confidence: 99%

Mechanisms of action of glatiramer acetate in multiple sclerosis

Neuhaus¹,

Farina²,

Wekerle³

et al. 2001

Neurology

240

123

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This information is current as ofhttp://www.neurology.org/content/56/6/702.full.html located on the World Wide Web at:The online version of this article, along with updated information and services, is rights reserved. Print Article abstract-Glatiramer acetate (GA, Copaxone [Teva Pharmaceuticals, Kansas City, MO], formerly known as copolymer-1) and interferon-(IFN)-␤ 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.

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