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Arch Neurol. 2005;62:858-859.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Glatiramer acetate (Copaxone; Teva Pharmaceuticals, North Wales, Pa) is a random polymer of glutamic acid, lysine, alanine, and tyrosine, and is of considerable interest for its ability to reduce the frequency of relapses in relapsing-remitting multiple sclerosis (MS).¹ Several mechanisms have been proposed to explain these findings. Lando et al² suggested that inhibition of clinical disease in an animal model of MS, experimental autoimmune encephalomyelitis, was due to suppressor cells because protection could be adoptively transferred from glatiramer acetate–treated mice. Early studies suggested that glatiramer acetate could inhibit antigen-specific responses through competition for major histocompatibility complex molecules.³ More recent work suggests that glatiramer acetate treatment of MS patients and mice with experimental autoimmune encephalitis has several potential mechanisms, although the favored one seems to be of inducing a shift in the balance of Th1 and Th2 cells.^4-5 However, the exact T-cell populations responsible for these shifts were not characterized immunophenotypically . . . [Full Text of this Article]

AUTHOR INFORMATION

Nitin J. Karandikar, MD, PhD; Michael K. Racke, MD

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ABSTRACT | FULL TEXT