Lack of apolipoprotein-E exacerbates experimental allergic encephalomyelitis.
Experimental autoimmune encephalomyelitis (EAE) was found to have a chronic and significantly worse course in apolipoprotein-E (apoE) deficient female mice when compared with matched controls. Disease measures compared included incidence of EAE (64% versus 31%, P < 0.05, chi2 test), maximal clinical score (average +/- SD 2.81 +/- 2.5 versus 0.75 +/- 1.1, P < 0.01, Mann-Whitney test) and mortality (27.3% versus 0%, P = 0.02, Mann-Whitney test and chi2 test). ApoE deficient mice had significantly increased lymphocyte proliferation responses to both myelin antigens and mitogens and significantly more infiltrating lesions in the central nervous system (CNS) in histopathology. Defective neuronal repair mechanisms and enhanced immune reactivity in apoE deficient mice may explain our findings. Clinical implications for MS are discussed.
Karussis
D
D
Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah Medical Center, Hebrew University, Jerusalem, Israel. karus@cc.huji.ac.il
Michaelson
D M
DM
Grigoriadis
N
N
Korezyn
A D
AD
Mizrachi-Koll
R
R
Chapman
S
S
Abramsky
O
O
Chapman
J
J
D000544:Alzheimer Disease / Q000276:immunology / Q000503:physiopathology; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics*; D002455:Cell Division / Q000276:immunology; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009103:Multiple Sclerosis / Q000276:immunology / Q000503:physiopathology*; D018417:Th1 Cells / Q000166:cytology
D001057:Apolipoproteins E