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Dissecting the Genetic Basis of Rheumatoid Arthritis in Mouse Models

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Rheumatoid Arthritis, RA, is a common polygenic multi-factorial chronic inflammatory disorder that involves complex interactions between genetic and environmental factors. Despite major advances, the aetiology of the disease is still not completely understood. In this post-genome era, the sequencing of the human and some murine genomes as well as advances in global screening technologies offer an opportunity to accelerate the search for new pathological pathways and to identify new therapeutic targets. Animal models of RA offer an opportunity to dissect the genetic basis of disease in a simplified genome and controlled environment with the aim of identifying new pathological pathways and thus new therapeutic targets. Linkage analysis in the mouse model has identified more than 60 Loci, controlling disease phenotypes, immune response and cytokines. This indicates that gene variations among inbred mice strains affect the disease and that those polymorphic genes could be potential therapeutic targets. However, progress in identification of susceptibility genes in mouse models is slow. The progress is hampered by the complexity of disease as well as the traditional genetic dissection strategies. In this post-genome era, the sequencing of the human and some murine genomes as well as advances in global screening technologies offer an opportunity to accelerate the progress.





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Keywords: Collagen Induced Arthritis; Epistasis; Genomics; Microarrays; Quantitative Trait Loci; Rheumatoid Arthritis; differential expression

Document Type: Research Article

Affiliations: Section of Immunogenetics, University of Rostock, Schillingallee 70, 18055 Rostock, Germany.

Publication date: October 1, 2006

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