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• W2019014467 abstract "Experimental autoimmune encephalomyelitis (EAE) was induced with myelin oligodendrocyte glycoprotein (MOG1–125) in CD4−/− and CD8−/− DBA/1 mice. Both gene-deleted mice developed clinical signs of EAE, albeit milder than in wild-type mice, suggesting that both CD4+ and CD8+ cells participate in disease development. Demyelination and inflammation in the central nervous system was reduced in the absence of CD8+ T cells. Antibody depletion of CD4+ cells completely protected CD8−/− mice from MOG-induced EAE while depletion of CD8+ cells in CD4−/− mice resulted in fewer EAE incidence compared to that in control antibody-treated mice. Antibody depletion of CD4+ cells in wild-type mice protected from EAE, but not depletion of CD8+ cells, although demyelination was reduced on removal of CD8+ T cells. Immunization with immunodominant MOG79–96 peptide led to EAE only in the presence of pertussis toxin (PT) in the inoculum. PT also triggered an earlier onset and more severe EAE in CD8−/− mice. We interpret our findings such that in an ontogenic lack of CD4+ T cells, EAE is mediated by CD8+ and elevated levels of αβCD4−CD8− cells, and that CNS damage is partly enacted by the activity of CD8+ T cells." @default.
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• W2019014467 date "2003-08-01" @default.
• W2019014467 modified "2023-10-13" @default.
• W2019014467 title "Comparing the pathogenesis of experimental autoimmune encephalomyelitis in CD4−/− and CD8−/− DBA/1 mice defines qualitative roles of different T cell subsets" @default.
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• W2019014467 doi "https://doi.org/10.1016/s0165-5728(03)00210-8" @default.
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