Recent insights into the mechanism of action of glatiramer acetate.
Author(s): Kala M, Miravalle A, Vollmer T
Affiliation(s): Division of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA. mrinalini.kala@chw.edu
Publication date & source: 2011-06, J Neuroimmunol., 235(1-2):9-17. Epub 2011 Mar 13.
Publication type: Research Support, Non-U.S. Gov't; Review
Glatiramer acetate (GA, Copaxone(R), co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells. Copyright (c) 2011 Elsevier B.V. All rights reserved.
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