Induction of Hyperacute Brain Inflammation and Demyelination by Activated Encephalitogenic T Cells and a Monoclonal Antibody Specific for a Myelin/Oligodendrocyte Glycoprotein
作者:
SchluesenerHermann J.,
LiderOfer,
SobelRaymond A.,
期刊:
Autoimmunity
(Taylor Available online 1989)
卷期:
Volume 2,
issue 3
页码: 265-273
ISSN:0891-6934
年代: 1989
DOI:10.3109/08916938909014690
出版商: Taylor&Francis
关键词: Demyelination;encephalitis;T-cells;antibody;myelin oligodendrocyte glycoprotein
数据来源: Taylor
摘要:
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.
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