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The Journal of Immunology, Vol 157, Issue 5 2186-2192, Copyright © 1996 by American Association of Immunologists
ARTICLES |
JA Encinas, MB Lees, RA Sobel, C Symonowicz, JM Greer, CL Shovlin, HL Weiner, CE Seidman, JG Seidman and VK Kuchroo
Center for Neurologic Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Experimental autoimmune encephalomyelitis (EAE), a model for human multiple sclerosis, is a T cell-mediated autoimmune disease that can be induced in experimental animals by immunization with myelin Ags. Inbred strains of mice show varying degrees of susceptibility to EAE, indicating that susceptibility is an inherited trait. To define the genetic factors that control susceptibility to EAE, we performed linkage analysis on the first backcross (BC1) between highly susceptible SJL/J mice and resistant B10.S mice, both of which are of the H-2s haplotype. Mice were immunized for disease with encephalitogenic myelin proteolipid protein peptide 139 to 151, and analysis was performed on 68 backcross mice showing the severe disease phenotype (disease score > or = 3)and 68 backcross mice of the resistant phenotype (no clinical or histologic signs of disease) using microsatellite markers covering >98% of the genome. We found the strongest linkage (p = 0.001) with clinical disease at two loci: one at the telomeric end of chromosome 2, and another near the center of chromosome 3. In addition, several other regions showing some evidence of linkage (p < or = 0.05) with clinical disease were found.
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A. A. Hurwitz, T. J. Sullivan, R. A. Sobel, and J. P. Allison Cytotoxic T lymphocyte antigen-4 (CTLA-4) limits the expansion of encephalitogenic T cells in experimental autoimmune encephalomyelitis (EAE)-resistant BALB/c mice PNAS, March 5, 2002; 99(5): 3013 - 3017. [Abstract] [Full Text] [PDF]
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