Rheumatoid arthritis (RA) is a polygenic autoimmune disease primarily affecting the synovial joints. Numerous animal models show similarities to RA in humans; some of them not only mimic the clinical phenotypes but also demonstrate the involvement of homologous genomic regions in RA. This paper compares corresponding non-MHC genomic regions identified in rodent and human genome-wide association studies (GWAS). To date, over 30 non-MHC RA-associated loci have been identified in humans, and over 100 arthritis-associated loci have been identified in rodent models of RA. The genomic regions associated with the disease are designated by the name(s) of the gene having the most frequent and consistent RA-associated SNPs or a function suggesting their involvement in inflammatory or autoimmune processes. Animal studies on rats and mice preferentially have used single sequence length polymorphism (SSLP) markers to identify disease-associated qualitative and quantitative trait loci (QTLs) in the genome of F2 hybrids of arthritis-susceptible and arthritis-resistant rodent strains. Mouse GWAS appear to be far ahead of rat studies, and significantly more mouse QTLs correspond to human RA risk alleles. 1. Introduction Rheumatoid arthritis (RA) is a polygenic systemic autoimmune disease that mainly affects the synovial joints, causing chronic inflammation and profound tissue destruction in affected patients. The pathological features of RA include leukocyte infiltration of the synovial tissue (mainly T cells and macrophages), autoantibody production (e.g., against immunoglobulins, citrullinated peptides, or tissue-restricted antigens), the accumulation of inflammatory cells (mainly neutrophils) in the joint fluid, the proliferation of synovial fibroblasts, and the formation of pannus; collectively, these features result in the destruction of articular cartilage and bone erosion. The identification of genetic alterations and variations in RA (involving either the major histocompatibility complex (MHC) or non-MHC genes) and an understanding of their functional consequences may impact the diagnosis, therapy, and prevention of RA [1], an autoimmune disease that affects approximately 1% of the human population. No other autoimmune disease appears in so many different clinical forms or is characterised by such heterogeneous and diverse clinical symptoms and laboratory tests. As a consequence, there are many experimental animal models attempting to mimic the multiple clinical symptoms of RA. Animal studies may help to fill the gaps in human genome-wide association studies
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