PMID: 2491610Jan 1, 1989Paper

Induction of hyperacute brain inflammation and demyelination by activated encephalitogenic T cells and a monoclonal antibody specific for a myelin/oligodendrocyte glycoprotein

Autoimmunity
H J SchluesenerR A Sobel

Abstract

CNS demyelinating inflammatory disease can be a multifactorial process mediated by cellular and antibody-mediated immune processes. Myelin basic protein (MBP)-specific T cells and pathogenic 8-18C5 antibody, specific for a myelin/oligodendrocyte glycoprotein (MOG), a minor component of CNS white matter, can coexist in rats without triggering disease. However, transfer of activated MBP-specific T-cells followed by the injection of 8-18C5 antibody resulted in hyperacute disease progression and CNS demyelination. Transfer of activated T cells specific for an irrelevant antigen or transfer of activated but irradiated encephalitogenic T cells did not induce disease in the presence of 8-18C5 antibody. When needle lesions were induced in brains of 8-18C5 antibody treated rats, no enhancement of demyelination was seen around the needle track. Thus, accessibility of the brain parenchyma to 8-18C5 antibody was not sufficient to induce local demyelination. Therefore, it appears that activated encephalitogenic T cells are involved in initiating the 8-18C5 antibody-mediated demyelinating process.

References

Jan 1, 1987·Immunogenetics·M F SeldinH C Morse
Mar 1, 1986·Journal of Neuroimmunology·H J Schluesener, H Lassmann
Sep 1, 1984·Journal of Neuroimmunology·C LinningtonP L Woodhams
Jan 1, 1984·The Journal of Clinical Investigation·J HoloshitzI R Cohen
Jan 1, 1983·Acta Neuropathologica. Supplementum·J Cervós-NavarroB J Mrsulja
Jan 1, 1983·Acta Neuropathologica. Supplementum·M W BrightmanJ Anders
Sep 1, 1982·Acta Physiologica Scandinavica·I Belova, G Jonsson
Dec 1, 1981·Proceedings of the National Academy of Sciences of the United States of America·R D Broadwell, M Salcman
Aug 1, 1982·Immunology Today·D W Bailey

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