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Mechanisms of damage and repair in multiple sclerosis — a reviewUniversity of Cambridge Neurology Unit, Addenbrooke's Hospital, Hill's Road, Cambridge CB2 2QQ, UK
University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hill's Road, Cambridge CB2 2QQ, UK Pathological features of MS include perivascular inflammation and demyelination with oligodendrocyte loss; in addition, attempts at remyelination are of ten unsuccessful and may culminate in astrocytic scarring. One approach to investigating the biological principles underlying these processes is to use in vitro systems to analyse single-cell behaviour as well as cell-cell interactions. This paper reviews such data concerned with cell injury and repair which illuminate both demyelination and remyelination. In tissue culture oligodendrocytes are susceptible to injury via cell-mediated and humoral mechanisms. Substances including complement and tumour necrosis factor are capable of killing rat oligodendrocytes in vitro; surface complement activation also initiates a number of intracellular processes within oligodendrocytes as well as providing ligands for phagocytic interactions. The reasons for oligodendrocyte complement activation are discussed, but it appears that species differences exist when extrapolating these data to humans. Myelination and remyelination can also be studied both in vitro and in vivo using defined cell populations. Results from these studies may eventually help to explain some pathological features of MS, including astrocytosis and factors governing the limits of remyelination.
Key Words: inflammation • complement • tumour necrosis factor • myelination • astrocytosis
Multiple Sclerosis, Vol. 1, No. 2,
61-72 (1995) This article has been cited by other articles:
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