title: 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.
authors.affiliation: Department of Neuropathology, University of Göttingen, Göttingen, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Kuhlmann
authors.forename: C
authors.initials: C
authors.lastname: Lucchinetti
authors.forename: U K
authors.initials: UK
authors.lastname: Zettl
authors.forename: A
authors.initials: A
authors.lastname: Bitsch
authors.forename: H
authors.initials: H
authors.lastname: Lassmann
authors.forename: W
authors.initials: W
authors.lastname: Brück
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D003711:Demyelinating Diseases / Q000473:pathology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D005260:Female; D019254:Genes, bcl-2 / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000378:metabolism; D009103:Multiple Sclerosis / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D009186:Myelin Sheath / Q000473:pathology; D009685:Nuclear Envelope / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2