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Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 284751, 14 pages
Review Article

Non-MHC Risk Alleles in Rheumatoid Arthritis and in the Syntenic Chromosome Regions of Corresponding Animal Models

1Department of Rheumatology, Faculty of Medicine, Medical and Health Science Centre, University of Debrecen, Debrecen 4012, Hungary
2Section of Molecular Medicine, Departments of Orthopedic Surgery, Biochemistry, and Rheumatology, Rush University Medical Center, Chicago, IL 60612, USA

Received 12 June 2012; Revised 13 August 2012; Accepted 30 September 2012

Academic Editor: Mohammed Tikly

Copyright © 2012 Timea Besenyei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.