title: Suppression of experimental allergic encephalomyelitis by COP1--relevance to multiple sclerosis.
abstract: The evidence in this presentation clearly indicates that in the case of the model disease EAE, desensitization procedures are effective in suppressing the symptoms of the disease and in providing protection against it. The antigens used in our studies are all synthetic materials immunologically relevant to the myelin encephalitogenic protein, but not encephalitogenic themselves. The most effective of these materials is a random basic copolymer of alanine, glutamic acid, lysine and tyrosine, denoted COP 1. The finding that the suppressive polymers show immunological cross-reactivity with the encephalitogenic protein provides a logical basis for the explanation of their suppressive activity in terms of an immunological desensitization mechanism. Our studies suggest that the effectiveness of COP 1 in preventing EAE results from the production of antigen-suppressor T cells, and/or from blocking MBP-specific effector T cells. The results of the clinical trial presented here show demonstrable improvement in the COP 1-treated patients as compared with the placebo subjects, particularly for those patients with less severe MS at the start of the treatment. Thus, although the evidence supporting the antigenic role of MBP in MS is not strong, COP 1, a synthetic polypeptide simulating some of the properties of MBP, appears to be effective in altering the course of MS and is of potential value as a modality for the treatment of this disease.
authors.affiliation: Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
authors.forename: R
authors.initials: R
authors.lastname: Arnon
authors.forename: D
authors.initials: D
authors.lastname: Teitelbaum
authors.forename: M
authors.initials: M
authors.lastname: Sela
mesh_terms: D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000517:prevention & control*; D006801:Humans; D009103:Multiple Sclerosis / Q000276:immunology / Q000517:prevention & control*; D010455:Peptides / Q000627:therapeutic use*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
chemical_list: D010455:Peptides; C021759:(T,G)-A-L