Abstract
EXPERIMENTAL allergic encephalomyelitis (EAE) is an acute neurological autoimmune disease induced in laboratory animals such as guinea-pigs, rabbits, rats and monkeys by administration in complete Freund's adjuvant of a basic encephalitogenic protein (BE) isolated from the brain or spinal cord of several animal species1. We have recently shown2 that the disease may be suppressed by intravenous injection of a synthetic amino-acid copolymer (denoted Cop 1). This copolymer is composed of alanine, glutamic acid, lysine and tyrosine, in a residue molar ratio of 6.0 : 1.9 : 4.7 : 1.0, and has an average molecular weight of 23,000. This basic polymer is not encephalitogenic2 and is not a general non-specific immunosuppressive agent (our unpublished results). Whereas it efficiently suppresses the disease when administered after the basic encephalitogen, it cannot prevent the disease when injected intravenously in saline before the basic brain protein2.
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TEITELBAUM, D., WEBB, C., MESHORER, A. et al. Protection against Experimental Allergic Encephalomyelitis. Nature 240, 564–566 (1972). https://doi.org/10.1038/240564b0
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DOI: https://doi.org/10.1038/240564b0
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