Background: One or more components of the oligodendrocyte-myelin unit are the target of immune attack in multiple sclerosis. The role of complement in this process has been suggested by the demonstration in vitro that rat oligodendrocytes are sensitive to lysis by Ab-independent complement attack, partly because of a lack of the complement regulatory protein molecule, CD59.
Experimental design: This study assessed the sensitivity in vitro of human oligodendrocytes derived from neurosurgical specimens to complement attack and analyzed CD59 expression on their surface. The presence of CD59 was also examined in the human central nervous system during myelination and in both the normal and diseased adult brain.
Results: Human oligodendrocytes are insensitive in vitro to complement attack in the absence of Ab and using the Ab YTH 53.1 and were shown to possess CD59 on their surface. CD59 is absent from the human central nervous system before myelination, at which stage strong expression occurs in areas of myelin production. CD59 expression is then normally down-regulated but is particularly strong in reactive astrocytes in diseases such as multiple sclerosis.
Conclusions: The findings suggest that the previous demonstration of rat oligodendrocyte complement sensitivity and lack of CD59 expression do not extend to the human central nervous system. There may be a role for CD59 in normal human myelination.