Abstract
The alteration in expression of major histocompatibility complex (MHC) class I genes on neural cells in association with central nervous system (CNS) demyelination was studied. Infection of mice or glial cell cultures with a neurotropic demyelinating coronavirus, mouse hepatitis virus (MHV) strain A59, was used as a model system. While uninfected neural cells do not express detectable amounts of MHC class I surface antigens, after infection with MHV-A59 in vitro or in vivo, these antigens can be detected by reaction with a monoclonal antibody against H-2D and H-2K. Induction of MHC class I antigens by MHV-A59 infection in mice was associated with increased levels of H-2 mRNA. Upregulation of MHC class I antigens involved the production of soluble factor/s produced by infected astrocytes. The identity of the factor, which is not interferon, is at present unknown. Brain specimens from autopsies of patients with multiple sclerosis, a human inflammatory demyelinating diseases, were also examined for alteration of MHC antigens. Both class I and class II surface antigens were found in active plaques but not in chronic plaques or in normal brain. These results are consistent with the hypothesis that MHC class I antigen induction may play a role in inflammatory CNS demyelination in both experimental animals and in humans.
Keywords
- Multiple Sclerosis
- Major Histocompatibility Complex
- Major Histocompatibility Complex Class
- Mouse Hepatitis Virus
- Major Histocompatibility Complex Antigen
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1987 Plenum Press, New York
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Lavi, E. et al. (1987). Expression of MHC Class I Genes in Mouse Hepatitis Virus (MHV-A59) Infection and in Multiple Sclerosis. In: Lai, M.M.C., Stohlman, S.A. (eds) Coronaviruses. Advances in Experimental Medicine and Biology, vol 218. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1280-2_26
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DOI: https://doi.org/10.1007/978-1-4684-1280-2_26
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