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From the Department of Pathology, University of Washington School of Medicine, Seattle, Washington; the Department of Microbiology, Baylor University College of Medicine, Houston, Texas; and the Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland
Abstract
Inhibition of EAE by neural extracts is specifically related to the encephalitogenic potential of these extracts. Encephalitogen-induced inhibition is most potent when intracutaneous injections of a water-in-oil emulsion are given before the challenge. The specificity and time relationships suggest an immunologic mechanism, but all attempts to identify antibodies to the encephalitogen have so far been negative. The resistance to the effects of whole body x-irradiation suggests that inhibition of EAE, like EAE itself, is due to the mechanisms underlying delayed-type hypersensitivity.
Footnotes
1 This investigation was supported in part by Research Grant B-3147 (formerly B-1283) from the National Institute of Neurological Diseases and Blindness, U. S. Public Health Service, and Research Grant 239 from the National Multiple Selerosis Society.
Presented in part at the 36th annual meeting of the American Association of Neuropathologists, Boston, June 11, 1960 (1).
2 Research Fellow of the National Multiple Sclerosis Society.
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