Shedding microvesicles released by a human microglial cell line (CHME-5): A good platform for studying the biology of the system

blocks NFκB translocation and NO production in astrocytes evoked by either S1P or inflammatory cytokines and this effect results in the inhibition of astrocyte-mediated neurodegeneration. Finally, therapeutic administration of Fingolimod to EAE mice hampers astrocyte activation and nitrosative stress in vivo. In conclusion these data indicate that neurotoxic mediators released by astrocytes following activation of S1P and cytokine signalling cascades may contribute to neuronal damage in MS via NFκB pathway activation and NO production, and that the neuroprotective effect of Fingolimod in vivo may be the indirect result of its action on astrocyte activation. This study was supported by Fondazione Italiana Sclerosi Multipla (FISM) (2012/R/7), Amici Centro Sclerosi Multipla (Acesm) and Italian Ministry of Health.