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Fingolimod ameliorates axonal damage in experimental autoimmune encephalomyelitis

Fingolimod (FTY) is a new oral drug for multiple sclerosis. It acts as a functional antagonist for sphingosine 1‐phosphate receptor (S1PR). After phosphorylateion by sphingosine kinase in vivo, FTY binds to S1PR on lymphocytes to downregulate S1PR, thereby preventing lymphocyte egress from lymphoid tissues to reduce infiltration of autoreactive lymphocytes into the central nervous system. FTY easily passes through the blood–brain barrier and directly affects cells in the central nervous system. Recently, we have shown that FTY exerts neuroprotective effects by suppressing pro‐inflammatory functions of glial cells and by upregulating neuroprotective functions of neuronal and glial cells in vitro. In the present study, we examined whether FTY exerts neuroprotective effects in vivo in the chronic phase of experimental autoimmune encephalomyelitis (EAE).