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Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
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Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
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Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice

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Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice
Journal Article

Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8$^{-/-}$ Mice

1992
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Overview
Mice lacking in CD8 were generated from homologous recombination in embryonal stem cells at the CD8 locus and bred with the experimental allergic encephalomyelitis (EAE)-susceptible PL/J H-2$^u$ through four backcross generations to investigate the role of CD8$^+$ T cells in this model of multiple sclerosis. The disease onset and susceptibility were similar to those of wild-type mice. However, the mutant mice had a milder acute EAE, reflected by fewer deaths, but more chronic EAE, reflected by a higher frequency of relapse. This suggests that CD8$^+$ T lymphocytes may participate as both effectors and regulators in this animal model.