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*
Department of Veterinary Pathobiology, University of Illinois, Urbana, IL 61802;
Department of Microbiology, Brigham Young University, Provo, UT 84602;
Department of Microbiology and Immunology, Allegheny University of the Health Sciences, Philadelphia, PA 19102;
§
Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107; and
¶
The Wellcome Trust Center for Human Genetics, Nuffield Department of Surgery, University of Oxford, Oxford, United Kingdom OX3 7BN
Experimental allergic encephalomyelitis (EAE), the principal animal model of multiple sclerosis, is a genetically determined phenotype. In this study, analyses of the cumulative disease frequencies in parental, F1 hybrid, and F2 mice, derived from the EAE-susceptible SJL/J strain and the EAE-resistant B10.S/DvTe strain, confirmed that susceptibility to EAE is not inherited as a simple Mendelian trait. Whole genome scanning, using 150 informative microsatellite markers and a panel of 291 affected and 390 unaffected F2 progeny, revealed significant linkage of EAE susceptibility to marker loci on chromosomes 7 (eae4) and 17, distal to H2 (eae5). Quantitative trait loci for EAE severity, duration, and onset were identified on chromosomes 11 (eae6, and eae7), 2 (eae8), 9 (eae9), and 3 (eae10). While each locus reported in this study is important in susceptibility or disease course, interactions between marker loci were not statistically significant in models of genetic control. One locus, eae7, colocalizes to the same region of chromosome 11 as Orch3 and Idd4, susceptibility loci in autoimmune orchitis and insulin-dependent diabetes mellitus, respectively. Importantly, eae5 and eae7 are syntenic with human chromosomes 6p21 and 17q22, respectively, two regions of potential significance recently identified in human multiple sclerosis genome scans.
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E. P. Blankenhorn, R. J. Butterfield, R. Rigby, L. Cort, D. Giambrone, P. McDermott, K. McEntee, N. Solowski, N. D. Meeker, J. F. Zachary, et al. Genetic Analysis of the Influence of Pertussis Toxin on Experimental Allergic Encephalomyelitis Susceptibility: An Environmental Agent Can Override Genetic Checkpoints J. Immunol., March 15, 2000; 164(6): 3420 - 3425. [Abstract] [Full Text] [PDF]
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K. Bergsteinsdottir, H.-T. Yang, U. Pettersson, and R. Holmdahl Evidence for Common Autoimmune Disease Genes Controlling Onset, Severity, and Chronicity Based on Experimental Models for Multiple Sclerosis and Rheumatoid Arthritis J. Immunol., February 1, 2000; 164(3): 1564 - 1568. [Abstract] [Full Text] [PDF]
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C. Teuscher, R. J. Butterfield, R. Z. Ma, J. F. Zachary, R. W. Doerge, and E. P. Blankenhorn Sequence Polymorphisms in the Chemokines Scya1 (TCA-3), Scya2 (Monocyte Chemoattractant Protein (MCP)-1), and Scya12 (MCP-5) Are Candidates for eae7, a Locus Controlling Susceptibility to Monophasic Remitting/Nonrelapsing Experimental Allergic Encephalomyelitis J. Immunol., August 15, 1999; 163(4): 2262 - 2266. [Abstract] [Full Text] [PDF]
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 J. T. Chang, E. M. Shevach, and B. M. Segal Regulation of Interleukin (IL)-12 Receptor {beta}2 Subunit Expression by Endogenous IL-12: A Critical Step in the Differentiation of Pathogenic Autoreactive T Cells J. Exp. Med., March 15, 1999; 189(6): 969 - 978. [Abstract] [Full Text] [PDF]
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R. J. Butterfield, E. P. Blankenhorn, R. J. Roper, J. F. Zachary, R. W. Doerge, J. Sudweeks, J. Rose, and C. Teuscher Genetic Analysis of Disease Subtypes and Sexual Dimorphisms in Mouse Experimental Allergic Encephalomyelitis (EAE): Relapsing/Remitting and Monophasic Remitting/Nonrelapsing EAE Are Immunogenetically Distinct J. Immunol., March 1, 1999; 162(5): 3096 - 3102. [Abstract] [Full Text] [PDF]
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J. J. Weis, B. A. McCracken, Y. Ma, D. Fairbairn, R. J. Roper, T. B. Morrison, J. H. Weis, J. F. Zachary, R. W. Doerge, and C. Teuscher Identification of Quantitative Trait Loci Governing Arthritis Severity and Humoral Responses in the Murine Model of Lyme Disease J. Immunol., January 15, 1999; 162(2): 948 - 956. [Abstract] [Full Text] [PDF]
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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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I. A. Eaves, L. S. Wicker, G. Ghandour, P. A. Lyons, L. B. Peterson, J. A. Todd, and R. J. Glynne Combining Mouse Congenic Strains and Microarray Gene Expression Analyses to Study a Complex Trait: The NOD Model of Type 1 Diabetes Genome Res., February 1, 2002; 12(2): 232 - 243. [Abstract] [Full Text] [PDF]
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