Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3064657 | Journal of Neuroimmunology | 2010 | 8 Pages |
Abstract
Accumulating evidence indicates that interferon-β (IFN-β) can modify the complex immunopathogenic scenario causing clinical relapse activity and disease progression in MS. However, the beneficial effects of IFN-β in MS patients may also depend on non-immune mechanisms, including the modulation of astrocyte function. In the present report, we have shown that, depending on the dose, IFN-β treatment can either promote astrocyte proliferation and survival, or result astrocyte death. These actions depend, at least in part, on the regulation of nuclear factor-kappa B (NF-κB), an inducible transcription factor present in neurons and glia. This bimodal effect of IFN-β adds a new layer of complexity in the actions of IFN-β within the CNS.
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Authors
Olga Barca, Pablo Devesa-Peleteiro, Marcos Seoane, Rosa Ma Señarís, Víctor M. Arce,