Bcl-2-expressing oligodendrocytes in multiple sclerosis lesions

Citation
T. Kuhlmann et al., Bcl-2-expressing oligodendrocytes in multiple sclerosis lesions, GLIA, 28(1), 1999, pp. 34-39
Citations number
32
Categorie Soggetti
Neurosciences & Behavoir
Journal title
GLIA
ISSN journal
08941491 → ACNP
Volume
28
Issue
1
Year of publication
1999
Pages
34 - 39
Database
ISI
SICI code
0894-1491(199910)28:1<34:BOIMSL>2.0.ZU;2-I
Abstract
Multiple sclerosis (MS)is a chronic inflammatory disease of the central ner vous system leading to selective destruction of myelin sheaths and/or oligo dendrocytes. The immunological mechanisms responsible for myelin destructio n and the primary target, of the immune response have not yet; been identif ied. Prior studies have reported a variable degree of oligodendrocyte prese rvation 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 associated proteins that protec ts cells from cell death. The purpose of the present study was to determine whether bcl-2 expression is associated with oligodendrocyte preservation o bserved in some early MS lesions. Double inmunocytochemistry was performed with antibodies against bcl-2 and myelin oligodendrocyte glycoprotein (MOG) to identify bcl-2-expressing oligodendrocytes within MS lesions from 43 pa tients. The number of bcl-2-positive oligodendrocytes was determined depend ing on the lesion demyelinating activity and the disease course of the pati ents. The number of bcl-2-expressing oligodendrocytes increased within demy elinating lesions compared to the periplaque white matter, with highest num bers in remyelinating lesions. There was a significant association between the presence of bcl-2-positive oligodendrocytes and the presence of remyeli nation. The highest proportion of bcl-2-positive oligodendrocytes was obser ved in a subgroup of patients with relapsing-remitting disease course. The expression of apoptosis-associated proteins may contribute to oligodendrocy te preservation or loss in MS lesions. (C) 1999 Wiley-Liss, Inc.