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

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.

journal_name

Autoimmunity

journal_title

Autoimmunity

authors

Schluesener HJ,Lider O,Sobel RA

doi

10.3109/08916938909014690

subject

Has Abstract

pub_date

1989-01-01 00:00:00

pages

265-73

issue

3

eissn

0891-6934

issn

1607-842X

journal_volume

2

pub_type

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