Interleukin-1β (IL-1β) is a proinflammatory cytokine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and viral infections of the CNS. However, we demonstrate here that IL-1β appears to promote remyelination in the adult CNS. InIL-1β^−/− mice, acute demyelination progressed similarly to wild-type mice and showed parallel mature oligodendrocyte depletion, microglia–macrophage accumulation, and the appearance of oligodendrocyte precursors. In contrast,IL-1β^−/− mice failed to remyelinate properly, and this appeared to correlate with a lack of insulin-like growth factor-1 (IGF-1) production by microglia–macrophages and astrocytes and to a profound delay of precursors to differentiate into mature oligodendrocytes. Thus, IL-1β may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia–macrophage-derived IGF-1.