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(American Journal of Pathology. 2004;164:363-369.)
© 2004 American Society for Investigative Pathology

Short Communication

Bystander CD8 T-Cell-Mediated Demyelination is Interferon--Dependent in a Coronavirus Model of Multiple Sclerosis

Ajai A. Dandekar^*, Daniela Anghelina and Stanley Perlman^*

From the Interdisciplinary Programs in Immunology^* and Neuroscience, and the Departments of Pediatrics and Microbiology, University of Iowa, Iowa City, Iowa

Mice infected with the coronavirus mouse hepatitis virus, strain JHM (JHM) develop a disease that shares many histological characteristics with multiple sclerosis. We previously demonstrated that JHM-infected mice that only have CD8 T cells specific for an epitope not in the virus develop demyelination on specific activation of these cells. Herein we show that this process of bystander T-cell-mediated demyelination is interferon- (IFN-)-dependent. The absence of IFN- abrogated demyelination but did not change T-cell infiltration or expression levels of inflammatory cytokines or chemokines in the spinal cord. These results are consistent with models in which IFN- contributes to CD8 T-cell-mediated demyelination by activation of macrophages/microglia, the final effector cells in the disease process.

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