IFN-β counteracts the apoptosis induced by TNF in astrocytes through stimulation of PI-3K and MEK

Although IFN-beta has been shown to have efficacy in the treatment of MS (multiple sclerosis), its mechanism of action remains unclear. Most of the effort in the study of the relevant mechanisms of IFN-beta has dealt with its ability to regulate immune function. However, nonimmune mechanisms may also contribute to its efficacy. In the present work, we have found that treatment of fetal astrocytes with TNF induces a significant increase in apoptotic cell death that can be counteracted by IFN-beta, through a mechanism that involves PI3K/Akt and MEK/ERK pathways. Since, it has been shown that both TNF and its receptors are up regulated in active MS lesions our finding raise the possibility that the beneficial effects of IFN-beta on MS treatment may depend, at least partially, on its ability to protect astrocytes against TNF-induced apoptosis.