Human brain astrocytes mediate TRAIL-mediated apoptosis after treatment with IFN-γ

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MeSH: Antineoplastic Agents/pharmacology* ; Apoptosis/drug effects* ; Apoptosis/physiology ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism* ; Astrocytes/cytology* ; Astrocytes/drug effects ; Astrocytes/metabolism ; Cells, Cultured ; Humans ; Interferon-gamma/pharmacology* ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism* ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism*

Abstract: TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1β, TNF-α or IFN-γ, TRAIL was induced in cultured fetal astrocytes. In particular, IFN-γ induced the highest levels of TRAIL in cultured astrocytes. When astrocytes were prereated with IFN-γ, they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-γ modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain.