Brines et al. have demonstrated that EPO mediates neuroprotection against experimental ischemic brain injury [164] . Agnello et al. have shown that EPO exerts an antiinflammatory effect that ameliorates EAE [165] . Yuan et al. also demonstrated that EPO retains its immunomodulatory capacity in both the periphery and the inflamed spinal cord by promoting a massive expansion of Treg cells, inhibiting Th17 polarization and abrogating the proliferation of antigen-presenting DCs [166] . We observed significantly reduced levels of both Th1 and Th17 cells in the CNS and a significantly increased proportion of splenic Tregs in EPOtreated Mog-EAE mice. We also demonstrated that MOGspecific T-cell proliferation was suppressed in the EPOtreated group [167] .