Glatiramer acetate

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Background

Glatiramer acetate (GA) is a selective inhibitor of cytokine production by immature DC [1].
IL-12p70 is a key factor secreted by sentinel DC driving Th1 responses. The chronic activation of Th1 cells results in immunopathology and organ-specific autoimmune disease.
GA selectively inhibits cytokine produced by tissue-type sentinel DC. Different increasing dose of GA is added to the immature DC activated by exposure to LPS in vitro. The secretion of IL-12p70 was inhibited by GA in a dose-dependent manner. The mature DC in the presence of GA can induce Th2 cells accompanied by high levels of IL-10, which prime DC for reduced IL-12p70 production [1].
Applying GA to mice of three stages of experimental autoimmune encephalomyelitis by 8 to 10 days (2 mg per mouse) showed the expression of BDNF, NT-3 and NT-4 are continuously increasing in specific brain regions. Even started 45 days after disease induction, GA treatment restored the level of NTs back to that of healthy mice [2].

Reference:
[1]. Wormmeester J, Vieira PL, Wierenga EA, et al. Glatiramer acetate (copolymer-1, Copaxone) promotes Th2 cell development and increased IL-10 production through modulation of dendritic cells. [J]. The Journal of Immunology: Official Journal of the American Association of Immunologists, 2003, 170(9): 4483-4488.
[2]. Eilam R, Aharoni R, Arnon R, et al. The immunomodulator glatiramer acetate augments the expression of neurotrophic factors in brains of experimental autoimmune encephalomyelitis mice. [J]. Proceedings of the National Academy of Sciences of the United States of America. , 2005, 102(52): 19045-19050.