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Bystander CD8 T-Cell-Mediated Demyelination is Interferon-γ -Dependent in a Coronavirus Model of Multiple Sclerosis
Journal article   Open access   Peer reviewed

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

Ajai A Dandekar, Daniela Anghelina and Stanley Perlman
American Journal of Pathology, Vol.164(2), pp.363-369
2004
DOI: 10.1016/S0002-9440(10)63126-4
PMCID: PMC1602263
PMID: 14742242
url
https://doi.org/10.1016/S0002-9440(10)63126-4View
Published (Version of record) Open Access

Abstract

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-gamma (IFN-gamma)-dependent. The absence of IFN-gamma 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-gamma contributes to CD8 T-cell-mediated demyelination by activation of macrophages/microglia, the final effector cells in the disease process.

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