Vesicular removal by oligodendrocytes of membrane attack complexes formed by activated complement (original) (raw)

Nature volume 339, pages 620–622 (1989)Cite this article

Abstract

OLIGODENDROCYTES synthesize myelin in the central nervous system and maintain it in lamellar sheaths around axons. Techniques for studying oligodendrocyte development _in vitro_1 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 sclerosis3–5and 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.

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Author notes

  1. D. A. S. Compston: To whom correspondence should be addressed at

Authors and Affiliations

  1. Section of Neurology,
    N. J. Scolding, C. Linington & D. A. S. Compston
  2. Department of Medical Biochemistry, University of Wales College of Medicine, Heath Park, Cardiff, CF4 4XN, UK
    B. P. Morgan, W. A. J. Houston & A. K. Campbell
  3. University of Cambridge Clinical School, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK
    D. A. S. Compston

Authors

  1. N. J. Scolding
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  2. B. P. Morgan
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  3. W. A. J. Houston
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  4. C. Linington
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  5. A. K. Campbell
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  6. D. A. S. Compston
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Scolding, N., Morgan, B., Houston, W. et al. Vesicular removal by oligodendrocytes of membrane attack complexes formed by activated complement.Nature 339, 620–622 (1989). https://doi.org/10.1038/339620a0

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