Oligodendroglial response to the immune cytokine interferon gamma

Brian Popko*, Kristine D. Baerwald

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

58 Scopus citations

Abstract

In the human demyelinating disorder multiple sclerosis, and its animal model experimental allergic encephalomyelitis, there is a breakdown of the blood-brain barrier and an infiltration of immune cells into the CNS. Infiltrating T lymphocytes and macrophages are believed to be key mediators of the disease process. Considerable circumstantial and experimental evidence has suggested that the pleiotropic cytokine interferon gamma (IFN-γ), which is exclusively expressed by T cells and natural killer cells, is a deleterious component of the immune response in these disorders. When experimentally introduced into the CNS IFN-γ promotes many of the pathological changes that occur in immune-mediated demyelinating disorders. In vitro, this cytokine elicits a number of effects on oligodendrocytes, including cell death. The harmful actions of IFN-γ on CNS myelin are likely mediated through direct effects on the myelinating cells, as well as through the activation of macrophages and microglia. In this review we summarize relevant studies concerning the action of IFN-γ in demyelinating disorders and discuss possible mechanisms for the observed effects.

Original languageEnglish (US)
Pages (from-to)331-338
Number of pages8
JournalNeurochemical Research
Volume24
Issue number2
DOIs
StatePublished - 1999

Keywords

  • Demyelination
  • Experimental allergic encephalomyelitis
  • Interferon gamma
  • MHC class I
  • Multiple sclerosis
  • Oligodendrocytes
  • Remyelination

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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