The findings suggest that CD8(+) T cells do not play a significant role in the pathogenesis or regulation of EAE induced by rMOG in DA rats. In this respect, rMOG-induced EAE is not an appropriate model for studying the role of CD8(+) T cells in MS.
Throughout the disease, both CD4(+) T cells and macrophages/activated microglia outnumbered CD8(+) T cells within the spinal cord. The number of putative suppressor CD8(+) T cells increased significantly both during and after the first peak suggesting the induction of a regulatory CD8(+) T-cell response. However, antibody-mediated depletion of CD8(+) T cells before induction of the disease, or after the first peak, did not significantly alter the incidence, severity or course of rMOG-induced EAE.
Since CD8(+) T cells may be important in the pathogenesis of multiple sclerosis (MS), we examined their role in the DA rat experimental autoimmune encephalomyelitis (EAE) model induced by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG).
The inflammatory infiltrate in the spinal cord of affected animals was assessed by histology, electrophysiology and flow cytometry during the course of the disease (the first peak, remission and the second peak). The proportions of activated/memory effector (CD8(+)CD44(+)) and putative suppressor (CD8(+)CD28(-), CD8(+)CD25(high)) CD8(+) T cells in the draining lymph nodes were determined. To explore the role of CD8(+) T cells, similar experiments were performed in CD8(+) T cell depleted rats, before, during and after the first peak of the disease.