Bcl-2-expressing oligodendrocytes in multiple sclerosis lesions.

Abstract:

:Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system leading to selective destruction of myelin sheaths and/or oligodendrocytes. The immunological mechanisms responsible for myelin destruction and the primary target of the immune response have not yet been identified. Prior studies have reported a variable degree of oligodendrocyte preservation in actively demyelinating lesions. We have previously demonstrated that oligodendrocyte survival is heterogenous and varies between individual MS patients. Bcl-2 belongs to the group of apoptosis-associated proteins that protects cells from cell death. The purpose of the present study was to determine whether bcl-2 expression is associated with oligodendrocyte preservation observed in some early MS lesions. Double immunocytochemistry was performed with antibodies against bcl-2 and myelin oligodendrocyte glycoprotein (MOG) to identify bcl-2-expressing oligodendrocytes within MS lesions from 43 patients. The number of bcl-2-positive oligodendrocytes was determined depending on the lesion demyelinating activity and the disease course of the patients. The number of bcl-2-expressing oligodendrocytes increased within demyelinating lesions compared to the periplaque white matter, with highest numbers in remyelinating lesions. There was a significant association between the presence of bcl-2-positive oligodendrocytes and the presence of remyelination. The highest proportion of bcl-2-positive oligodendrocytes was observed in a subgroup of patients with relapsing-remitting disease course. The expression of apoptosis-associated proteins may contribute to oligodendrocyte preservation or loss in MS lesions.

journal_name

Glia

journal_title

Glia

authors

Kuhlmann T,Lucchinetti C,Zettl UK,Bitsch A,Lassmann H,Brück W

subject

Has Abstract

pub_date

1999-10-01 00:00:00

pages

34-9

issue

1

eissn

0894-1491

issn

1098-1136

pii

10.1002/(SICI)1098-1136(199910)28:1<34::AID-GLIA4>

journal_volume

28

pub_type

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