Am J Pathol. 2004 Feb;164(2):363-9
Dandekar AA, Anghelina D, Perlman S.
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-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.