Cell type-specific regulation of major histocompatibility complex (MHC) class I gene expression in astrocytes, oligodendrocytes, and neurons

Glia. 1993 Jul;8(3):201-7. doi: 10.1002/glia.440080307.


Mechanisms of major histocompatibility complex (MHC) class I gene regulation in cells of the CNS have been studied in vitro. Astrocytes in primary cultures, but neither oligodendrocytes nor neurons, constitutively expressed cell surface MHC class I molecules. Interferon-gamma (IFN-gamma) treatment led to induction of MHC class I expression in astrocytes and oligodendrocytes but not in neurons. The conserved upstream sequence containing the juxtaposed nuclear factor (NF)-kappa B-like region I and IFN-response consensus sequence (ICS) constitutively enhanced MHC class I gene promoter activity in astrocytes, but not in oligodendrocytes or in neurons. Nuclear extracts from astrocytes, but not from oligodendrocytes and neurons, had a binding activity specific for the NF-kappa B-like region I sequence, indicating that constitutive expression of MHC class I genes is governed by the upstream region I enhancer and its binding factor. IFN-gamma treatment led to induction of MHC class I promoter activity in astrocytes and oligodendrocytes, but not in neurons. In accordance with this observation, a nuclear factor that binds to the ICS was induced in astrocytes and oligodendrocytes but not in neurons following IFN-gamma treatment. This study illustrates cell type-specific regulation of MHC class I genes in the CNS that correlates with the expression of DNA binding factors relevant to MHC class I gene transcription.

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / drug effects
  • Astrocytes / immunology
  • Astrocytes / metabolism*
  • Base Sequence
  • Cells, Cultured
  • Consensus Sequence
  • DNA-Binding Proteins / metabolism
  • Enhancer Elements, Genetic
  • Gene Expression Regulation* / drug effects
  • Genes, MHC Class I*
  • Genes, Synthetic
  • H-2 Antigens / biosynthesis*
  • Interferon-gamma / pharmacology
  • Mice
  • Molecular Sequence Data
  • NF-kappa B / metabolism
  • Nerve Tissue Proteins / biosynthesis*
  • Neurons / drug effects
  • Neurons / immunology
  • Neurons / metabolism*
  • Oligodendroglia / drug effects
  • Oligodendroglia / immunology
  • Oligodendroglia / metabolism*
  • Organ Specificity
  • Promoter Regions, Genetic


  • DNA-Binding Proteins
  • H-2 Antigens
  • NF-kappa B
  • Nerve Tissue Proteins
  • Interferon-gamma