Copaxone review article (may require subscription), reference below.
It goes over the various observed effects, as an altered peptide ligand, effect on regualtory T cells, APCs, and various clinical studies.
Whatever the case, change in doses and schedules of immunomodulators can have major consequences, so i cannot imagine how the 40mg producte would not require extensive studies.
Excert:
Possible mechanisms of action of GA. GA acts directly on APC to modify them into noninflammatory type II cells (1). GA is processed by APC (2) through class I (cross-presentation; 3) and class II (4) presentation pathways and is presented to CD8+ and CD4+ T cells, respectively. A robust CD8+ T cell response is either enhanced by or results in killing/modification of APC subsets (5). Presentation by modified APC results in generation of CD4+ Treg (6). Direct killing of Th1 CD4+ T cells results in deviation toward Th2 responses (7).
J Immunol. 2011 Feb 15;186(4):1887-90.
Glatiramer acetate treatment of multiple sclerosis: an immunological perspective.
Racke MK, Lovett-Racke AE.
Department of Neurology, The Ohio State University Medical Center, Columbus, OH 43210.
Abstract
Glatiramer acetate (GA) has been used as an immunomodulatory agent for the treatment of relapsing-remitting multiple sclerosis (MS) in the United States since 1996. It is currently one of two first-line agents for use in the treatment of relapsing-remitting MS. GA was the first agent to be used in the treatment of MS that was developed using the animal model of MS called experimental autoimmune encephalomyelitis. In this commentary, we examine the development of GA as a treatment for MS and discuss its mechanism of action as suggested by recent studies using modern immunologic methods.
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