Abstract
Microglia have been proposed to play a pathogenetic role in immunologically mediated neurodegenerative diseases. In our study, using microglial/neuronal cell cocultures primed with IFN-γ, we found that both LPS and TNF-α triggered neuronal cell injury (impairment of γ-aminobutyric acid uptake and neuronal loss) via a nitric oxide mechanism. Pretreatment of cell cocultures with IL-4, an immunosuppressive cytokine, prevented, in a dose-dependent manner, neuronal cell injury induced by activated microglia. The mechanism by which IL-4 exerts its neuroprotective effect was found to involve the inhibition of IFN-γ priming of microglia with a subsequent decrease in the production of TNF-α and nitric oxide.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1473-1481 |
| Number of pages | 9 |
| Journal | Journal of Immunology |
| Volume | 151 |
| Issue number | 3 |
| State | Published - Aug 1 1993 |
