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Role of IFN-γ responsiveness in CD8 T cell-mediated viral clearance and demyelination in coronavirus-infected mice

Steven P. Templeton,S. Perlman

Published 2007 in Journal of Neuroimmunology

ABSTRACT

Immunocompetent, but not RAG1−/− mice infected with MHV–JHM develop demyelination. Transferred CD8 T cell-enriched splenocytes reconstitute demyelination, and this ability is dependent on donor IFN-γ. We used IFN-γR1−/− mice to examine the target of IFN-γ in CD8 T cell-mediated demyelination. In IFN-γR1−/−RAG1−/− recipients, demyelination is decreased, but not eliminated, while viral titers are significantly increased when compared to IFN-γR1+/+RAG1−/− recipients. IFN-γR1−/− CD8 T cells retain virus-specific effector function regardless of IFN-γR1 expression. Although IFN-γR1 responsiveness is critical for maximal demyelination, increased levels of infectious virus coupled with adoptive transfer of CD8 T cells may result in myelin destruction independent of IFN-γR1 expression.

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