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We hypothesized that disease-specific variants exclusively associated with only one disease could contribute to disease-specific phenotypes. We calculated the strength of disease specificity for each variant in each disease against the other disease using summary association statistics reported in the largest genome-wide association studies of RA and SLE. Most of highly disease-specific associations were explained by non-coding variants that were significantly enriched within regulatory regions (enhancers or H3K4me3 histone modification marks) in specific cell or organ types. (e.g., In RA, regulatory T primary cells, CD4+ memory T primary cells, thymus and lung; In SLE, CD19+ B primary cells, mobilized CD34+ primary cells, regulatory T primary cells and monocytes). Consistently, genes in the disease-specific loci were significantly involved in T cell- and B cell-related gene sets in RA and SLE. In summary, this study identified disease-specific variants between RA and SLE, and provided statistical evidence for disease-specific cell types, organ and gene sets that may drive the disease-specific phenotypes.<\/jats:p>","DOI":"10.1038\/s41598-019-39132-2","type":"journal-article","created":{"date-parts":[[2019,2,25]],"date-time":"2019-02-25T11:03:08Z","timestamp":1551092588000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Genetic variants differentially associated with rheumatoid arthritis and systemic lupus erythematosus reveal the disease-specific biology"],"prefix":"10.1038","volume":"9","author":[{"given":"Jiwoo","family":"Lim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8926-6216","authenticated-orcid":false,"given":"Kwangwoo","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,2,25]]},"reference":[{"key":"39132_CR1","doi-asserted-by":"publisher","first-page":"373","DOI":"10.1038\/gene.2009.39","volume":"10","author":"KL Moser","year":"2009","unstructured":"Moser, K. 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