In rodent models, extensive spontaneous remyelination and functional recovery is possible after an episode of acute transient demyelination (4, 5) . Proliferation of immature cells and differentiation into myelinating oligodendrocytes is required for this extensive remyelination (6, 7) . Similarly, immature oligodendrocyte lineage cells persist in the adult human CNS and may proliferate to increase in number within and near MS lesions (8, 9) . However, these immature cells often fail to differentiate sufficiently to remyelinate throughout the extent of MS lesions. Therefore, the repair capacity of endogenous cells may be limited by nonpermissive signals in chronic MS lesions.