Abstract
Growing evidence from epidemiological studies indicates the association between rheumatoid arthritis (RA) and measles. However, the exact mechanism for this association is still unclear now. We consider that the strong association between both diseases may be caused by shared genetic pathways. We performed a pathway analysis of large-scale RA genome-wide association studies (GWAS) dataset with 5,539 cases and 20,169 controls of European descent. Meanwhile, we evaluated our findings using previously identified RA loci, protein-protein interaction network and previous results from pathway analysis of RA and other autoimmune diseases GWAS. We confirmed four pathways including Cytokine-cytokine receptor interaction, Jak-STAT signaling, T cell receptor signaling and Cell adhesion molecules. Meanwhile, we highlighted for the first time the involvement of Measles and Intestinal immune network for IgA production pathways in RA. Our results may explain the strong association between RA and measles, which may be caused by the shared genetic pathway. We believe that our results will be helpful for future genetic studies in RA pathogenesis and may significantly assist in the development of therapeutic strategies.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammatory polyarthritis [1]
We found that all the pathway analyses used the Wellcome Trust Case-Control Consortium (WTCCC) or North American Rheumatoid Arthritis Consortium (NARAC) dataset or both datasets [3,14,15,16,17,18,19,20]
Identifying rheumatoid arthritis (RA) risk pathways by hypergeometric test We investigated the enrichment of RA genes identified by VEGAS and RA susceptibility genes identified by previous genome-wide association studies (GWAS)
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammatory polyarthritis [1]. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, about 1.3 million adults in the U.S suffer from RA [3]. RA is a complex disease caused by a combination of genetic susceptibility and environmental factors [4]. Much effort has been devoted to finding common RA variants; especially genome-wide association studies (GWAS) [4,5,6,7,8,9]. These known genetic factors just explain 50–60% of the genetic variance for susceptibility to ACPA-positive and 30–50% susceptibility for ACPA-negative RA [10]. Considering the complex genetic architecture, it is apparent that additional risk variants remain to be discovered
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