Less mortality but more relapses in experimental allergic encephalomyelitis in CD8-/- mice.
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/JH-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.
Koh
D R
DR
Department of Medical Biophysics, University of Toronto, Princess Margaret Hospital, Canada.
Fung-Leung
W P
WP
Ho
A
A
Gray
D
D
Acha-Orbea
H
H
Mak
T W
TW
D000818:Animals; D016827:CD8 Antigens / Q000235:genetics* / Q000378:metabolism; D003433:Crosses, Genetic; D004261:DNA Replication; D003643:Death; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D007376:Interleukin-2 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D009103:Multiple Sclerosis / Q000276:immunology / Q000503:physiopathology; D012016:Reference Values; D013601:T-Lymphocytes / Q000276:immunology*; D013936:Thymidine / Q000378:metabolism
D016827:CD8 Antigens; D007376:Interleukin-2; D013936:Thymidine