Differential regulation of major histocompatibility complex class II expression and nitric oxide release by β-amyloid in rat astrocyte and microglia

Tamas Pazmany, Laszlo Mechtler, Thomas B. Tomasi, Janos P. Kosa, Andrea Turoczi, Zoltan Urbanyi

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2 Citations (Scopus)


Astrocytes and microglial cells were examined for expression of two immunologically important molecules, major histocompatibility complex class II (MHC-II) and nitric oxide (NO) following treatment with IFN-γ and β- amyloid (βA) peptides, βA(1-42) and βA(25-35). IFN-γ is a potent inducer of both MHC-II gene expression and NO production. The induction of MHC-II was inhibited by both βA peptides in astrocytes but they had little or no effect in microglia, βA peptides had no effect on NO release in astrocytes but on microglia βA(1-42) synergistically induced NO release with IFN-γ. Transient transfection of astrocytes with 5' deletional mutants of MHC-II IAα promoter linked to the chloramphenicol acetyl transferase reporter gene (IAα-CAT), demonstrated that βA acts at the transcriptional level to downregulate IFN- γ induced MHC-II gene expression in astrocytes. In previous studies, the induction of MHC-II on glial cells were suggested to be involved in the pathogenesis of neurodegenerative diseases and MHC-II+ microglial cells were observed at much higher frequency than astrocytes. This study provides information on the regulation of the MHC-II gene expression in astrocytes and in microglial cells by βA and this pathway may be critically involved in the immune/inflammatory regulation within the central nervous system.

Original languageEnglish
Pages (from-to)213-223
Number of pages11
JournalBrain research
Issue number2
Publication statusPublished - Jul 24 1999



  • Alzheimer's disease
  • Astrocyte
  • MHC-II
  • Microglia
  • NO
  • β-amyloid

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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