Multiple sclerosis

Oligodendrocytes in active lesions do not express class II major histocompatibility complex molecules

Sunhee C. Lee, Cedric S. Raine

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

The expression of major histocompatibility complex (MHC) molecules by oligodendrocytes has been proposed as evidence for their involvement in the multiple sclerosis (MS) lesion although the literature on the subject is controversial and based largely upon observations in vitro. With a modified immunocytochemical procedure on 1 μm epoxy sections, the present study has examined the expression of class II MHC molecules (Ia) on cells within actively demyelinating lesions in a central nervous system biopsy from a case of acute MS. White Ia was readily demonstrable on microglial cells aand astrocytes, it was never detected on adjacent surviving oligodendrocytes. Unexpectedly, in parallel sectios, the oligodendrocytes stained positively for myelin-associated glycoprotein, a marker for immature oligodendrocytes. The unequivocal lack of Ia expression by oligodendrocytes in MS makes it unlikely that they serve as immunomodulators in lesion pathogenesis.

Original languageEnglish (US)
Pages (from-to)261-266
Number of pages6
JournalJournal of Neuroimmunology
Volume25
Issue number2-3
DOIs
StatePublished - 1989

Fingerprint

Oligodendroglia
Major Histocompatibility Complex
Multiple Sclerosis
Myelin-Associated Glycoprotein
Immunologic Factors
Astrocytes
Central Nervous System
Biopsy

Keywords

  • Demyelination
  • Major histocompatibility complex clas II
  • Multiple sclerosis
  • Myelin-associated glycoprotein
  • Oligodendrocyte
  • Plaque
  • Remyelination

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Clinical Neurology
  • Neurology

Cite this

Multiple sclerosis : Oligodendrocytes in active lesions do not express class II major histocompatibility complex molecules. / Lee, Sunhee C.; Raine, Cedric S.

In: Journal of Neuroimmunology, Vol. 25, No. 2-3, 1989, p. 261-266.

Research output: Contribution to journalArticle

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