{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:10:37Z","timestamp":1790813437132,"version":"4.1.0"},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2019,9,1]],"date-time":"2019-09-01T00:00:00Z","timestamp":1567296000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Beh\u00e7et disease is a chronic, relapsing-remitting autoinflammatory syndrome with a strong HLA-B*51 association. In this paper, we describe a human cohort of 267 individuals with Beh\u00e7et disease and 445 matched controls from a tertiary referral center in the U.K. HLA-B*51 was confirmed as a genetic risk factor in this group (p = 0.0006, Bonferroni\u2013Dunn correction for multiple testing [Pc] = 0.0192, odds ratio [OR] 1.92, 95% confidence interval [CI] 1.33\u20132.76). KIR3DL1\/S1 allele-level analysis indicated that low-expressing KIR3DL1\/S1 alleles in combination with KIR3DS1 increased the risk of developing Beh\u00e7et disease (KIR3DL1LOW\/KIR3DS1: p = 0.0004, Pc = 0.0040, OR 2.47, 95% CI 1.43\u20134.25), whereas high-expressing KIR3DL1\/S1 alleles in combination with a null-expressing KIR3DL1 reduced the risk of disease (KIR3DL1HIGH\/KIR3DL1NULL: p = 0.0035, Pc = 0.0350, OR 0.53, 95% CI 0.33\u20130.87). Beh\u00e7et disease can manifest as a purely mucocutaneous disease or can involve other organ systems such as the eyes. In the U.K. cohort studied in this study, KIR3DL1LOW\/KIR3DS1 increased the risk of ophthalmic disease (p = 1.2 \u00d7 10\u22125, OR 3.92, 95% CI 2.06\u20137.47), whereas KIR3DL1HIGH\/KIR3DL1NULL reduced the risk of having purely mucocutaneous disease (p = 0.0048, OR 0.45, 95% CI 0.25\u20130.81). To our knowledge, this is the first analysis of KIR3DL1\/S1 allelic variation in Beh\u00e7et disease and may provide insight into the pathogenic role of HLA-B*51 and its interaction with KIR3DL1\/S1.<\/jats:p>","DOI":"10.4049\/jimmunol.1801178","type":"journal-article","created":{"date-parts":[[2019,8,12]],"date-time":"2019-08-12T18:24:02Z","timestamp":1565634242000},"page":"1629-1635","source":"Crossref","is-referenced-by-count":22,"title":["KIR3DL1\/S1 Allotypes Contribute Differentially to the Development of Beh\u00e7et Disease"],"prefix":"10.1093","volume":"203","author":[{"given":"Harry","family":"Petrushkin","sequence":"first","affiliation":[{"name":"Moorfields Eye Hospital National Health Service Foundation Trust, Medical Retina Department , London EC1V 2PD ,","place":["United Kingdom"]},{"name":"Clinical and Diagnostic Oral Sciences, Queen Mary University of London, Blizard Institute , E1 2AT London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8370-7703","authenticated-orcid":false,"given":"Paul J","family":"Norman","sequence":"additional","affiliation":[{"name":"Division of Biomedical Informatics and Personalized Medicine, Department of Microbiology and Immunology, University of Colorado , Aurora, CO 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emma","family":"Lougee","sequence":"additional","affiliation":[{"name":"Viapath, Clinical Transplantation Laboratory, Guy\u2019s Hospital, Guy\u2019s and St Thomas\u2019 National Health Service Foundation Trust , London SE1 9RT ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Parham","sequence":"additional","affiliation":[{"name":"Department of Structural Biology, Stanford University School of Medicine , Stanford, CA 94305"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2054-0509","authenticated-orcid":false,"given":"Graham R","family":"Wallace","sequence":"additional","affiliation":[{"name":"Centre for Translational Inflammation Research, University of Birmingham Research Laboratories, Queen Elizabeth Hospital, University of Birmingham , Birmingham B15 2TT ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miles R","family":"Stanford","sequence":"additional","affiliation":[{"name":"Medical Eye Unit, St Thomas\u2019 Hospital, Guy\u2019s and St Thomas\u2019 National Health Service Foundation Trust , London SE1 7EH ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5930-1973","authenticated-orcid":false,"given":"Farida","family":"Fortune","sequence":"additional","affiliation":[{"name":"Clinical and Diagnostic Oral Sciences, Queen Mary University of London, Blizard Institute , E1 2AT London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,9,15]]},"reference":[{"key":"2025030417541943900_r1","doi-asserted-by":"crossref","first-page":"213","DOI":"10.1034\/j.1399-0039.1999.540301.x","article-title":"Beh\u00e7et\u2019s disease, the Silk Road and HLA-B51: historical and geographical perspectives","volume":"54","author":"Verity","year":"1999","journal-title":"Tissue Antigens"},{"issue":"5","key":"2025030417541943900_r2","first-page":"S125","article-title":"Prevalence of Adamantiades-Beh\u00e7et\u2019s disease in Germany and the municipality of Berlin: results of a nationwide survey","volume":"24","author":"Papoutsis","year":"2006","journal-title":"Clin. 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