Abstract
Inflammatory demyelination and failure of remyelination are features of multiple sclerosis. A number of in vitro studies have demonstrated that cultured oligodendrocytes are damaged and even killed by serum factors such as complement, inflammatory cytokines and products of activated macrophages1,2. These mediators of inflammation can gain access to the CNS when there is breakdown of the blood-brain barrier. This has led to the suggestion that breakdown of the blood-brain barrier and/or inflammation alone may be sufficient to bring about CNS demyelination, and some have even suggested that such events may be crucially involved in the pathogenesis of multiple sclerosis.
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References
K. Selmaj, C.S. Raine, M. Farooq, W.T. Norton and C.S. Brosnan, Cytokine cytotoxicity against oligodendrocytes.Apoptosis induced by lymphotoxin, J. Immunol 147: 1522 (1991).
A. Compston, N. Scolding, D. Wren amd M. Noble, The pathogenesis of demyelinating disease: insights from cell biology, TINS, 14: 175 (1991).
W.F. Blakemore and A.J. Crang, The relationship between type-1 astrocytes, Schwann cells and oligodendrocytes following transplanation of glial cell cultures into demyelinating lesions in the adult rat spinal cord. J. Neurocytol., 18: 519 (1989).
A.J. Crang and W.F. Blakemore, The effect of the number of oligodendrocytes transplanted into x-irradiated, glial-free lesions on the extent of oligodendrocyte remyelination. Neurosci. Lett., 193: 269 (1989).
R.J.M. Franklin, A.J. Crang and W.F. Blakemore, Type-1 astrocytes fail to inhibit Schwann cell remyelination of CNS axons in the absence of cells of the O-2A lineage. Devel. Neurosci., 14: 85 (1992).
D.L. Graca and W.F. Blakemore, Delayed remyelination in rat spinal cord following ethidium bromide injection. Neuropathol. Appl. Neurobiol., 12: 593 (1986).
R.J.M. Franklin, A.J. Crang and W.F. Blakemore, Transplanted type-1 astrocytes facilitate repair of demyelinating lesions by host oligodendrocytes in adult rat spinal cord. J. Neurocytol, 20: 420 (1991).
A.J. Crang and W.F. Blakemore, Remyelination of demyelinated rat axons by transplanted mouse oligodendrocytes. Glia, 4: 305 (1991).
A.R. Harvey, Y. Fan, M.W. Beilharz and M.D. Grounds, Survival and migration of transplanted male glia in adult female mouse brains monitored by a Y-chromosome-specific probe. Mol.Brain.Res., 12: 339 (1992).
W.F. Blakemore and A.J. Crang, The use of cultured autologous Schwann cells to remyelinate areas of persistent demyelination in the central nervous system, J. Neurol. Sci., 70: 207 (1985).
RJ.M. Franklin, A.J. Crang and W.F. Blakemore, The reconstruction of an astrocytic environment in glia-deficent areas of white matter, J. Neurocytol, in press (1993).
S.K. Ludwin, Chronic demyelination inhibits remyelination in the central nervous system, Lab. Invest., 43: 382 (1980).
C.S. Raine, Multiple sclerosis: immunolopathologic mechanisms in the progression and resolution of inflammatory demyelination, In Mechanisms in Neurologic and Psychriatiric Disease Ed. B.H. Waksman Raven press New York, p 37 (1990).
E.N. Benveniste and J.A. Merrill, Stimulation of oligodendroglial proliferation and maturation by interleukin-2, Nature, 321: 610 (1986).
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Blakemore, W.F., Crang, A.J. (1994). Areas of Demyelination Repaired by Mouse Oligodendrocytes and Rat Type-1 Astrocytes Create a New Model of Immune Mediated Demyelination. In: Salvati, S. (eds) A Multidisciplinary Approach to Myelin Diseases II. NATO ASI Series, vol 258. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2435-9_19
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DOI: https://doi.org/10.1007/978-1-4615-2435-9_19
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