{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T17:58:28Z","timestamp":1783792708790,"version":"3.55.0"},"reference-count":50,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,4,19]],"date-time":"2018-04-19T00:00:00Z","timestamp":1524096000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Laboratory of Molecular and Cellular Genetic and Sciences and Technology University of Oran"},{"name":"Mohamed Boudiaf Resources"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J Immunogenetics"],"published-print":{"date-parts":[[2018,6]]},"abstract":"Summary<\/jats:title>Ankylosing spondylitis (AS<\/jats:styled-content>) is a complex inflammatory disease that represents a major health problem both in Algeria and worldwide. Several lines of evidence support that genetic risk factors play a role in AS<\/jats:styled-content> etiology and the CTLA<\/jats:styled-content>4<\/jats:italic> gene has attracted a considerable attention. In this study, we were interested in evaluating the HLA<\/jats:styled-content>\u2010B27<\/jats:italic> frequency and in exploring the CTLA<\/jats:styled-content>4<\/jats:italic> gene in a sample of the North African population. The dataset of the current study is composed of 81 patients with AS<\/jats:styled-content> and 123 healthy controls. All samples were genotyped by TaqMan\u00ae<\/jats:sup>allelic discrimination assay. The genetic risk of the HLA<\/jats:styled-content>\u2010B27<\/jats:italic> specificity and the CTLA<\/jats:styled-content>4\/CT<\/jats:styled-content>60<\/jats:italic> polymorphism were assessed by odds ratios (OR<\/jats:styled-content>) with 95% confidence intervals (CI<\/jats:styled-content>). High spondylitis risk was detected for HLA<\/jats:styled-content>\u2010B27<\/jats:italic> allele (OR<\/jats:styled-content>= 14.62, p\u00a0<\/jats:italic>=\u00a0<\/jats:italic>10\u22126<\/jats:sup>) in addition to a significant association of the CT<\/jats:styled-content>60<\/jats:italic>*G allele (OR<\/jats:styled-content>= 1.89, p\u00a0<\/jats:italic>=\u00a0<\/jats:italic>.002). After gender and age stratifications, the association of the CT<\/jats:styled-content>60<\/jats:italic>*G allele was still significant in females sample (OR<\/jats:styled-content>= 2.10, p\u00a0<\/jats:italic>=\u00a0<\/jats:italic>.001) and when age up to 30\u00a0years (OR<\/jats:styled-content> = 2.21, p\u00a0<\/jats:italic>=\u00a0<\/jats:italic>.008). Interestingly, the CT<\/jats:styled-content>60<\/jats:italic>*G allele revealed an increased spondylitis risk in the B27 negative group (OR<\/jats:styled-content>= 2.81, p\u00a0<\/jats:italic>=\u00a0<\/jats:italic>.006). The present work showed in West Algerian population that the HLA<\/jats:styled-content>\u2010B27<\/jats:italic> antigen and the variation in the CTLA<\/jats:styled-content>4<\/jats:italic> 3\u2032UTR<\/jats:styled-content> region played an important role in the ankylosing spondylitis susceptibility. The heterogeneity of this disease is deduced by genetic difference found between B27+ and B27\u2212 groups.<\/jats:p>","DOI":"10.1111\/iji.12369","type":"journal-article","created":{"date-parts":[[2018,4,20]],"date-time":"2018-04-20T04:35:18Z","timestamp":1524198918000},"page":"109-117","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Association of the HLA<\/scp>\u2010B27 antigen and the CTLA<\/scp>4<\/i> gene CT<\/scp>60\/rs3087243<\/i> polymorphism with ankylosing spondylitis in Algerian population: A case\u2013control study"],"prefix":"10.1111","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9529-2936","authenticated-orcid":false,"given":"C. A.","family":"Dahmani","sequence":"first","affiliation":[{"name":"Laboratoire de G\u00e9n\u00e9tique Mol\u00e9culaire et Cellulaire (LGMC) Universit\u00e9 des Sciences et de la Technologie d'Oran\u2010Mohamed Boudiaf (USTO\u2010MB) Oran Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Benzaoui","sequence":"additional","affiliation":[{"name":"Service de Rhumatologie Centre Hospitalo\u2010Universitaire (CHU) d'Oran Oran Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Amroun","sequence":"additional","affiliation":[{"name":"Laboratoire d'Immunog\u00e9n\u00e9tique et de Transplantation D\u00e9partement d'Immunologie Institut Pasteur d'Alg\u00e9rie \u00e0 Alger Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Mecabih","sequence":"additional","affiliation":[{"name":"Laboratoire d'Immunog\u00e9n\u00e9tique et de Transplantation D\u00e9partement d'Immunologie Institut Pasteur d'Alg\u00e9rie \u00e0 Alger Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F. Z.","family":"Sediki","sequence":"additional","affiliation":[{"name":"Laboratoire de G\u00e9n\u00e9tique Mol\u00e9culaire et Cellulaire (LGMC) Universit\u00e9 des Sciences et de la Technologie d'Oran\u2010Mohamed Boudiaf (USTO\u2010MB) Oran Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Zemani\u2010Fodil","sequence":"additional","affiliation":[{"name":"Laboratoire de G\u00e9n\u00e9tique Mol\u00e9culaire et Cellulaire (LGMC) Universit\u00e9 des Sciences et de la Technologie d'Oran\u2010Mohamed Boudiaf (USTO\u2010MB) Oran Algeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Fodil","sequence":"additional","affiliation":[{"name":"Laboratoire de G\u00e9n\u00e9tique Mol\u00e9culaire et Cellulaire (LGMC) Universit\u00e9 des Sciences et de la Technologie d'Oran\u2010Mohamed Boudiaf (USTO\u2010MB) Oran 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