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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.
Methods: We review the various mechanisms that have been proposed for this random polymer over the years, with emphasis on recent methods that utilize modern immunologic techniques.
Results: Studies describing processes such as immune deviation and effects on regulatory T cells and antigen-presenting cells are presented.
Conclusions: Effects of glatiramer acetate on the immune response have evolved as our technical abilities and knowledge of the immune response itself have developed.
Glossary
- APC=
- antigen-presenting cells;
- APL=
- altered peptide ligand;
- Cop-1=
- copolymer-1;
- EAE=
- experimental autoimmune encephalomyelitis;
- GA=
- glatiramer acetate;
- IFN=
- interferon;
- IL=
- interleukin;
- MBP=
- myelin basic protein;
- MHC=
- major histocompatibility complex;
- MS=
- multiple sclerosis;
- RRMS=
- relapsing-remitting multiple sclerosis;
- Th=
- T helper;
- TNF=
- tumor necrosis factor;
- Treg=
- T regulatory.
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