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From the Section on Myelin Chemistry, Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014, the Department of Pathology, New York Medical College Center for Chronic Disease, Bird S. Coler Hospital, Welfare Island, New York, New York 10017 and the Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195
Abstract
Central nervous system myelin basic proteins of various vertebrates, mammalian and submammalian, have been examined for encephalitogenic activity in guinea pigs and Lewis rats. Myelin basic proteins from mammalian, avian (chicken), reptilian (turtle) and amphibian (frog) species were encephalitogenic in rats at a level of 50 µg; those of fish (carp, shark) were completely inactive. None of the myelin basic proteins from the submammalian species was encephalitogenic in guinea pigs at levels as high at 250 µg. Guinea pigs responded equally well to 5 µg of all mammalian myelin basic proteins tested except the smaller of the two rat proteins, which was completely inactive at this level. In contrast, rats responded well to guinea pig and both the larger and the smaller rat proteins, but not as well to proteins of the other mammals (bovine, rabbit and human) at a 10-µg level. The different patterns of reactivity of guinea pigs and rats to mammalian and submammalian myelin basic proteins suggest that the two species recognize different amino acid sequences in the basic protein molecule as being encephalitogenic determinants. Additional studies carried out in highly susceptible strains of rats showed that whole spinal cord tissue of salamanders, as well as frog, is encephalitogenic, but that carp spinal cord is not. Evidence of rapid autolytic changes in spinal cord tissue from cold-blooded animals together with the observed heterogeneity of fish basic proteins indicate the need for caution in interpretation of negative results with carp and shark proteins.
Footnotes
1 Section on Myelin Chemistry, Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, Maryland 20014.
2 Department of Pathology, New York Medical College Center for Chronic Disease, Bird S. Coler Hospital, Welfare Island, New York, N. Y. 10017; supported in part by National Multiple Sclerosis Society Grant 536C12.
3 Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195; supported in part by United States Public Health Service, National Institutes of Health Grant NS-03147-12 and National Multiple Sclerosis Society Grant 427E12.
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