Abstract
IT is generally believed that experimental allergic encephalomyelitis results from an interaction between nervous tissue antigens and cells which are engaged in a delayed hypersensitive response. Although experimental allergic encephalomyelitis can be followed by circulating antibodies that react in vitro with nervous tissue constituents, all experiments designed to transfer passively experimental allergic encephalomyelitis either with sera from diseased animals or with antibrain immune sera have failed1. This has been taken as evidence that antibody does not play any significant part in the development of experimental demyelinating disease2. A possible explanation for the failure of antibrain antibodies to induce encephalomyelitic lesions may be their inability to cross the blood-brain barrier in sufficient amount. In order to test the role of antibrain antibodies in the pathogenesis of experimental allergic encephalomyelitis, guinea-pigs with a cannula inserted permanently into the lateral ventricle of the brain were used in the present experiment. Administration of serum through the cannula by-passes the blood-brain barrier, and permits direct contact of injected antibodies and nervous tissue.
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JANKOVIĆ, B., DRAŠKOCI, M. & JANJIĆ, M. Passive Transfer of ‘Allergic’ Encephalomyelitis with Antibrain Serum injected into the Lateral Ventricle of the Brain. Nature 207, 428–429 (1965). https://doi.org/10.1038/207428a0
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DOI: https://doi.org/10.1038/207428a0
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