CEREBROSPINAL-FLUID CONCENTRATIONS OF THE COMPLEMENT MAC INHIBITOR CD59 IN MULTIPLE-SCLEROSIS AND PATIENTS WITH OTHER NEUROLOGICAL DISORDERS

Rodent oligodendrocytes have a unique susceptibility among glia to the lytic effects of complement, due in part to a deficiency in CD59 (pro tectin), a key surface inhibitor of the complement membrane attack com plex (MAC). The possibility that shedding of CD59 by human oligodendro cytes contributes to complement-mediated oligodendrocyte injury in inf lammatory demyelinating disease has been investigated by estimating le vels of CD59 in cerebrospinal fluid samples from 12 patients with demy elinating disease of the central nervous system and 13 with other neur ological diseases. No significant differences were found between patie nts and controls, or between patients with active and those with clini cally inactive demyelinating disease, providing no direct support for oligodendrocyte shedding of CD59 in multiple sclerosis.