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.
KeywordsHepatitis Retina Resis Neurol Sine
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