{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,13]],"date-time":"2026-06-13T02:52:18Z","timestamp":1781319138952,"version":"3.54.1"},"reference-count":56,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2020,1,3]],"date-time":"2020-01-03T00:00:00Z","timestamp":1578009600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Tunisian Ministry of Higher Education and Scientific Research, Tunisia"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J Immunogenetics"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Autoimmune thyroid diseases (AITD) including Graves' disease (GD) and Hashimoto's thyroiditis (HT) are complex genetic diseases. Th2 cytokines act on the development of AITD. This study was conducted on Tunisian patients with AITD to investigate the association of Th2 cytokine gene polymorphisms and haplotype combination with GD or HT risk. A total of 156 controls, 160 patients with HT and 88 patients with GD were genotyped for IL\u20104 rs2243250, IL\u20105 rs2069812, IL\u20106 rs1800796 and IL\u201013 rs1800925 polymorphisms by PCR\u2010RFLP. The AITD risk was assessed by a logistic regression analysis using the SNP stats statistical program. False\u2010positive report probability (FPRP) was estimated to evaluate significant findings. IL\u201013 rs1800925 was associated with GD, after adjustment for age and gender, in codominant, dominant and allele genetic models (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.0072; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.0018; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.012, respectively). Significant association of the IL\u20106 rs1800796C\/G genotype with GD was also detected (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.025). Furthermore, increased risk of HT was still found for IL\u201013 rs1800925T allele (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.039, OR\u00a0=\u00a01.39) and for IL\u20104 rs2243250T\/T genotype both in codominant (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.033, OR\u00a0=\u00a02.59) and recessive (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.011, OR\u00a0=\u00a02.73) models after adjustment for age and gender. Interestingly, haplotype analysis performed on the IL\u20104, IL\u20105 and IL\u201013 genes revealed a high risk of HT with CTT haplotype (<jats:italic>p<\/jats:italic>\u00a0=\u00a0.008, OR\u00a0=\u00a02.12). However, the CCT haplotype is a protective factor (OR\u00a0=\u00a00.36). Patients carrying the CT haplotype with only one minor allele had a moderate risk of HT (OR\u00a0=\u00a01.56). The FPRP analysis showed that the association of IL\u201013 rs1800925 polymorphism with GD and HT and the association of CTT haplotype with HT were noteworthy. In conclusion, the IL\u20104, IL\u20105, IL\u20106 and IL\u201013 polymorphism may play a role in susceptibility to GD and HT in the Tunisian population. Furthermore, gene\u2013gene interaction between the IL\u20104, IL\u20105 and IL\u201013 significantly increases the risk of AITD. Further studies with larger numbers of individuals are needed to confirm the results.<\/jats:p>","DOI":"10.1111\/iji.12472","type":"journal-article","created":{"date-parts":[[2020,1,4]],"date-time":"2020-01-04T06:35:10Z","timestamp":1578119710000},"page":"294-308","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Association of cytokine Th2 gene polymorphisms with autoimmune thyroid diseases in Tunisian population"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3199-9040","authenticated-orcid":false,"given":"Souhir","family":"Mestiri","sequence":"first","affiliation":[{"name":"Laboratory of Genetics, Biodiversity and Bioresource Valorization Superior Institute of Biotechnology of Monastir University of Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7944-1604","authenticated-orcid":false,"given":"Ines","family":"Zaaber","sequence":"additional","affiliation":[{"name":"Laboratory of Genetics, Biodiversity and Bioresource Valorization Superior Institute of Biotechnology of Monastir University of Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oumaima","family":"Inoubli","sequence":"additional","affiliation":[{"name":"Laboratory of Genetics, Biodiversity and Bioresource Valorization Superior Institute of Biotechnology of Monastir University of Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nabil","family":"Abid","sequence":"additional","affiliation":[{"name":"Laboratory of Transmissible Diseases and Biological Active Substances LR99ES27 Faculty of Pharmacy University of Monastir Monastir Tunisia"},{"name":"Department of Biotechnology High Institute of Biotechnology of Sidi Thabet University Manouba Ariana\u2010Tunis Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abir","family":"Omrani","sequence":"additional","affiliation":[{"name":"Laboratory of Genetics, Biodiversity and Bioresource Valorization Superior Institute of Biotechnology of Monastir University of Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hana","family":"Nejehi","sequence":"additional","affiliation":[{"name":"Laboratory of Genetics, Biodiversity and Bioresource Valorization Superior Institute of Biotechnology of Monastir University of Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hela","family":"Marmouch","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine\u2010Endocrinology Hospital Fattouma Bourguiba in Monastir Monastir Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,1,3]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.3889\/oamjms.2016.110"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1530\/eje.1.02063"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.2003.01880.x"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(88)90152-8"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.12.8633"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(90)90452-Z"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/jcla.20152"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-007-9027-9"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1101\/gr.7.5.495"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1089\/thy.2012.0514"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1007\/s12020-015-0759-7"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-12-3488"},{"issue":"8","key":"e_1_2_7_14_1","first-page":"3861","article-title":"No association of an interleukin 4 gene promoter polymorphism with Graves' disease in the United Kingdom","volume":"86","author":"Heward J. 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