The mechanism of action of glatiramer acetate treatment in multiple sclerosis
- 5 January 2010
- journal article
- review article
- Published by Ovid Technologies (Wolters Kluwer Health) in Neurology
- Vol. 74 (1_suppleme), S25-S30
- https://doi.org/10.1212/wnl.0b013e3181c97e39
Abstract
Objective: Glatiramer acetate (formerly known as copolymer 1) is the major noninterferon immunomodulatory agent used in the treatment of relapsing-remitting multiple sclerosis. Its mechanism of action over the past 40 years has evolved with our understanding of the immune response.Keywords
This publication has 30 references indexed in Scilit:
- Transient regulatory T-cells: A state attained by all activated human T-cellsClinical Immunology, 2007
- Clinical response to glatiramer acetate correlates with modulation of IFN-γ and IL-4 expression in multiple sclerosisMultiple Sclerosis Journal, 2007
- Glatiramer acetate (GA) therapy induces a focused, oligoclonal CD8+ T-cell repertoire in multiple sclerosisJournal of Neuroimmunology, 2006
- CD28−CD57+ T cells predominate in CD8 responses to glatiramer acetateJournal of Neuroimmunology, 2006
- Multiple sclerosis: glatiramer acetate inhibits monocyte reactivity in vitro and in vivoBrain, 2004
- Glatiramer acetate-specific T-helper 1- and 2-type cell lines produce BDNF: implications for multiple sclerosis therapyBrain, 2002
- Glatiramer acetate (Copaxone®) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosisJCI Insight, 2000
- Intramuscular interferon beta‐1a for disease progression in relapsing multiple sclerosisAnnals of Neurology, 1996
- Copolymer 1 reduces relapse rate and improves disability in relapsing‐remitting multiple sclerosisNeurology, 1995
- A Pilot Trial of Cop 1 in Exacerbating–Remitting Multiple SclerosisThe New England Journal of Medicine, 1987