Oligodendrocytes and the Immune System
The existence of a common and frequently disabling human neurologic disease, multiple sclerosis (MS), which is characterized pathologically by inflammation (the hallmark of immune response) and demyelination within the central nervous system (CNS), has focussed interest on whether and how immune-mediated mechanisms can induce the observed tissue injury (Table 1). Inflammation and demyelination are also the hallmarks of acute disseminated encephalomyelitis (ADEM), a uniphasic disorder commonly encountered after immunization with nervous system-containing vaccines (e.g. Pasteur vaccine for rabies prevention) or specific exanthematous viral infections (measles) in which immune sensitization to myelin constituents can be demonstrated (Johnson et al., 1984). The more recently defined human disorder, HTLV-1-associated myelopathy (HAM) or tropical spastic paraparesis (TSP) is associated with oligodendrocyte (OGC)/myelin and axonal destruction and development of viral protein-directed cytotoxic lymphocytes; persistent virus is not yet detectible at the site of tissue injury within the CNS, invoking the postulate that immune-mediated mechanisms rather than direct viral mechanisms are involved (Moore et al., 1989). Similar considerations may apply to cases of CNS demyelination associated with HIV infection. Progressive multifocal leukoencephalopathy (PML), which most frequently occurs in immunocompromised individuals, provides a precedent for direct viral injury of OGC.
KeywordsMultiple Sclerosis Major Histocompatibility Complex Myelin Basic Protein Progressive Multifocal Leukoencephalopathy Experimental Allergic Encephalomyelitis
Unable to display preview. Download preview PDF.
- Arnold, D.L., Matthews, P.M., Francis, G.S., O’Connor, J., and Antel, J.P., 1992, Proton magnetic resonance spectroscopic imaging for metabolic characterization of demyelinating plaques, Ann. Neurol. 31: 235.Google Scholar
- Freedman M.S., Ruijs, T.C.G., and Antel JP, 1991b, The role of heat shock proteins in oligodendrocyte 7/8 cell interaction, J. Neuroimmunol. (Suppl 1 ): 112, 1991.Google Scholar
- Freedman, M.S., Ruijs, T.C.G., and Antel, J.P., Differential expression of heat shock proteins by human glial cells, J. Neuroimmunol.,in press.Google Scholar
- Griot, C., Vandevelde, M., Richard, A., Peterhans, E., and Stocker, R., 1990, Selective degeneration of oligodendrocytes mediated by reactive oxygen species, Free Rad. Res. Commns. 11: 4.Google Scholar
- Pette, M., Liebert, U.G., Toyka, K.V., and Hartung, H.P., 1992, Measles virus (MV)-specific T lymphocytes from MS patients and healthy donors, Neurology, 42 (Suppl. 3): 299.Google Scholar
- Ruijs, T.C.G., Freedman, M.S., Grenier, Y.G., Olivier, A., and Antel, J.P., 1990a, Human oligodendrocytes are susceptible to cytolysis by major histocompatibility complex class I-restricted lymphocytes, J. Neuroimmunol., 27: 89–97, 1990.Google Scholar
- Ruijs, T.C.G., Louste, K., Brown, E.A., and Antel, J.P., Lysis of human oligodendrocytes by MHCunrestricted CD4+ cytotoxic lymphocytes, J. Neuroimmunol., in press.Google Scholar
- Schluesener, H., Sobel, R., Linington, C., and Weiner, H., 1987, A monoclonal antibody against a myelin oligodendrocyte glycoprotein induces relapses and demyelination in CNS autoimmune disease, J. Immun!. 39: 4016.Google Scholar
- Wang, F.I., Stohlman, S.A., and Fleming, J.O., 1990, Demyelination induced by murine hepatitis virus JHM strain (MHV-4) is immunologically mediated, J. Neuroimmunol. 30–31.Google Scholar
- Weber, W.E.J., and Buurman, W.A., 1989, In vitro functional blocking of myelin basic protein-specific cytolytic human T lymphocyte clones by immunosuppressive drugs and monoclonal antibodies, J. Neuroimmunol. 22: 1.Google Scholar
- Williams, K., Bar-Or, A., Ulvestad, E., Olivier, A., Antel, J.P., and Yong, V.W., Biology of adult human microglia in culture: comparisons with peripheral blood monocytes and astrocytes, J. Neuropathol. Exp. Neurol., 51: 538.Google Scholar