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The Journal of Immunology, 2000, 164: 1564-1568.
Copyright © 2000 by The American Association of Immunologists

Evidence for Common Autoimmune Disease Genes Controlling Onset, Severity, and Chronicity Based on Experimental Models for Multiple Sclerosis and Rheumatoid Arthritis1

Kristin Bergsteinsdottir2,*, Hai-Tao Yang2,{dagger}, Ulf Pettersson{dagger} and Rikard Holmdahl3,*

* Section for Medical Inflammation Research, Lund University, Lund, Sweden; and {dagger} Department of Genetics and Pathology, Unit of Medical Genetics, Biomedical Center, Uppsala University, Uppsala, Sweden

The pathogenicity of multiple sclerosis is still poorly understood, but identification of susceptibility genes using the animal model experimental allergic encephalomyelitis (EAE) could provide leads. Certain genes may be shared between different autoimmune diseases, and identification of such genes is of obvious importance. To locate gene regions involved in the control of EAE and to compare the findings with the susceptibility loci recently identified in a model for rheumatoid arthritis (pristane-induced arthritis), we made crosses between the encephalomyelitis- and arthritis-susceptible rat strain DA and the resistant E3 strain. Genetic analysis of animals produced in a F2 intercross identified 11 loci associated with specific EAE-associated traits. Interestingly, five of these loci were situated at the same position as major loci controlling pristane-induced arthritis and showed similarities in inheritance pattern and subphenotype associations. Our results show that different phases of EAE are controlled by different sets of genes and that common genes are likely to be involved in different autoimmune diseases.




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