OLIGODENDROCYTES synthesize myelin in the central nervous system and maintain it in lamellar sheaths around axons. Techniques for studying oligodendrocyte development in vitro¹ can be used, indirectly, to investigate the myelin injury that occurs in human and experimental demyelinating disease². Cell-mediated immune mechanisms are necessary but not sufficient to induce myelin damage in vivo; more recently complement has also been implicated in the pathogenesis both of multiple sclerosis^3–5and experimental allergic encephalomyelitis⁶. Previously we have demonstrated that antibody-independent complement activation occurs in vitro at the oligodendrocyte surface⁷. Here we show that the ensuing oligodendrocyte injury is reversible, and that recovery involves the release of membrane-attack complex-enriched vesicles from the surface of viable cells. The demonstration of morphologically and immunochemically identical vesicles in the cerebrospinal fluid of patients with multiple sclerosis suggests that reversible complement-mediated injury contributes to myelin damage in vivo.