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- W4313350084 abstract "Abstract Pro-inflammatory cytokine-induced cell death of oligodendrocytes (OLs) is associated with axonal loss in neurodegenerative disorders including multiple sclerosis (MS) and that contributes to clinical exacerbation in affected individuals. Accumulating evidence suggest that both Th1 phenotype cytokine including tumor necrosis factor (TNF)-α and Th17 phenotype cytokine, interleukin (IL)-17 participate equally in MS pathogenesis. Here, we investigated the effect of IL-17 on OLs survival in the presence/absence of TNF-α in vitro. Our findings suggest that OL survival was not affected by IL-17 alone, but it exacerbated the TNF-α-induced OL apoptosis in a dose dependent fashion. Synergistic effect of these cytokines was ascribed to an inhibition of cell survival mechanisms, co-localization of Bid/Bax proteins in the mitochondrial membrane and caspase 8 activation mediated release of apoptosis inducing factor from mitochondria in OLs. In addition, cytokine treatment disturbed the mitochondrial membrane potential in OLs with corresponding increase in the generation of reactive oxygen species, which were attenuated by N-acetyl cysteine. Collectively, these data provide initial evidence that IL-17 exacerbates TNF-α-induced apoptotic cell death of OLs that antioxidant-based therapies have potential to limit CNS demyelination in MS or other related demyelinating disorders." @default.
- W4313350084 created "2023-01-06" @default.
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- W4313350084 date "2011-04-01" @default.
- W4313350084 modified "2023-09-26" @default.
- W4313350084 title "Interleukin-17 exacerbates tumor necrosis Factor-α induced apoptotic cell death of oligodendrocytes (148.8)" @default.
- W4313350084 doi "https://doi.org/10.4049/jimmunol.186.supp.148.8" @default.
- W4313350084 hasPublicationYear "2011" @default.
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