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Science 22 May 1992:
Vol. 256. no. 5060, pp. 1210 - 1213
DOI: 10.1126/science.256.5060.1210
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Articles

Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8-/- Mice

Dow-Rhoon Koh 1, Wai-Ping Fung-Leung 1, Alexandra Ho 1, Dawn Gray 1, Hans Acha-Orbea 2, and Tak-Wah Mak 1

1 Ontario Cancer Institute, Departments of Medical Biophysics and Immunology, University of Toronto, Princess Margaret Hospital, 500 Sherbourne Street, Toronto, Canada M4X 1 K9
2 Ludwig Institute for Cancer Research, Lausanne Branch, 1066 Epalinges, Switzerland

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-2u 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.


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Requirement for CD8+ cells in T cell receptor peptide-induced clonal unresponsiveness.
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Science 259, 91-94
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Role of CD8+ T Cells in Murine Experimental Allergic Encephalomyelitis.
H. Jiang, S.-l. Zhang, and B. Pernis (1992)
Science 256, 1213-1215
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CD8+ T cells are not necessary for 1alpha ,25-dihydroxyvitamin D3 to suppress experimental autoimmune encephalomyelitis in mice.
T. F. Meehan and H. F. DeLuca (2002)
PNAS 99, 5557-5560
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