{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T06:24:08Z","timestamp":1777875848148,"version":"3.51.4"},"reference-count":27,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T00:00:00Z","timestamp":1635724800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Thyroid\u00ae"],"published-print":{"date-parts":[[2021,11]]},"abstract":"\n Background:<\/jats:title>\n \n Vitamin A is a factor that suppresses immune responses, including T helper (Th)1 and Th17 responses. However, there has been no report showing the association between vitamin A-related genes (\n CYP26B1<\/jats:italic>\n ,\n RARB<\/jats:italic>\n , and\n RARG<\/jats:italic>\n ) and the prognosis of autoimmune thyroid disease (AITD). The objective of this study was to clarify the association between vitamin A-related genes and the susceptibility and prognosis of AITD.\n <\/jats:p>\n <\/jats:sec>\n \n Methods:<\/jats:title>\n We genotyped polymorphisms in genes encoding vitamin A-related molecules using the polymerase chain reaction-restriction fragment length polymorphism method. The proportion of T helper cells was analyzed by flow cytometry. Serum interleukin (IL)-17 and interferon (IFN)-\u03b3 were examined by enzyme-linked immunosorbent assay.<\/jats:p>\n <\/jats:sec>\n \n Results:<\/jats:title>\n \n CYP26B1<\/jats:italic>\n rs3768641 GG genotype and G allele were significantly more frequent in patients with mild Hashimoto's thyroiditis (HT) than in those with severe HT (\n p<\/jats:italic>\n \u2009=\u20090.0013 and 0.0024, respectively). The\n RARB<\/jats:italic>\n rs1997352 CC genotype was significantly more frequent in HT patients than in controls (\n p<\/jats:italic>\n \u2009=\u20090.0207). The proportion of Th17 cells was significantly higher in\n CYP26B1<\/jats:italic>\n rs2241057 TT genotype than C carrier (CC+CT genotypes) (\n p<\/jats:italic>\n \u2009=\u20090.0385), in\n RARB<\/jats:italic>\n rs1997352\u2009A carrier (AA+AC genotypes) than those with CC genotype (\n p<\/jats:italic>\n \u2009=\u20090.0246), and in\n RARG<\/jats:italic>\n rs7398676 G carrier (GG+GT genotypes) than in TT genotype (\n p<\/jats:italic>\n \u2009=\u20090.0249). In the\n RARB<\/jats:italic>\n rs1997352 polymorphism, HT patients with a high concentration of IFN-\u03b3 (\u2265150\u2009ng\/mL) were more frequent in the CC genotype than in A carriers (AA+AC genotypes) (\n p<\/jats:italic>\n \u2009=\u20090.0226). Serum levels of IL-17 were significantly elevated in subjects with the TT genotype of the\n CYP26B1<\/jats:italic>\n rs2241057 single nucleotide polymorphism (SNP) (\n p<\/jats:italic>\n \u2009=\u20090.0026) and in subjects with the GG genotype of the\n CYP26B1<\/jats:italic>\n rs3798641 SNP (\n p<\/jats:italic>\n \u2009=\u20090.030). Subjects with a high concentration of IL-17 (\u22650.71\u2009pg\/mL) were more frequent in\n RARG<\/jats:italic>\n 7398676 G carriers (GG+GT genotypes) than in TT genotype (\n p<\/jats:italic>\n \u2009=\u20090.0218).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions:<\/jats:title>\n \n Polymorphisms in the\n CYP26B1<\/jats:italic>\n gene were related to the proportion of Th17 cells, the level of IL-17 and the severity of HT. Polymorphisms in\n RAR<\/jats:italic>\n were related to the proportion of Th17 cells, concentrations of IFN-\u03b3 and IL-17, and susceptibility to HT.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1089\/thy.2021.0312","type":"journal-article","created":{"date-parts":[[2021,9,2]],"date-time":"2021-09-02T03:34:48Z","timestamp":1630553688000},"page":"1749-1756","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":6,"title":["Polymorphisms in Vitamin A-Related Genes and Their Functions in Autoimmune Thyroid Disease"],"prefix":"10.1177","volume":"31","author":[{"given":"Hinako","family":"Homma","sequence":"first","affiliation":[{"name":"Division of Health Sciences, Department of Biomedical Informatics, Osaka University Graduate School of Medicine, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5971-9296","authenticated-orcid":false,"given":"Mikio","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Division of Health Sciences, Department of Biomedical Informatics, Osaka University Graduate School of Medicine, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naoya","family":"Inoue","sequence":"additional","affiliation":[{"name":"Division of Health Sciences, Department of Biomedical Informatics, Osaka University Graduate School of Medicine, Osaka, Japan."},{"name":"Laboratory for Clinical Investigation, Osaka University Hospital, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Moeko","family":"Isono","sequence":"additional","affiliation":[{"name":"Division of Health Sciences, Department of Biomedical Informatics, Osaka University Graduate School of Medicine, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoh","family":"Hidaka","sequence":"additional","affiliation":[{"name":"Laboratory for Clinical Investigation, Osaka University Hospital, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4371-0398","authenticated-orcid":false,"given":"Yoshinori","family":"Iwatani","sequence":"additional","affiliation":[{"name":"Division of Health Sciences, Department of Biomedical Informatics, Osaka University Graduate School of Medicine, Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2021,11,10]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.autrev.2014.01.013"},{"key":"e_1_3_3_3_2","first-page":"243","article-title":"The immunopathogenesis of chronic autoimmune thyroiditis one century after Hashimoto","volume":"1","author":"Weetman AP","year":"2013","unstructured":"Weetman AP. 2013. The immunopathogenesis of chronic autoimmune thyroiditis one century after Hashimoto. Eur Thyroid J, 1:243\u2013250.","journal-title":"Eur Thyroid J"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200010263431707"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1089\/thy.2007.0170"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.3109\/08916934.2015.1134507"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1507\/endocrj.EJ16-0551"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10875-012-9721-0"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1507\/endocrj.K06-015"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2007.099739"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1089\/thy.2008.0423"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1515\/cmble-2015-0004"},{"key":"e_1_3_3_13_2","first-page":"375","article-title":"Transcriptional activity of TGFbeta1 and its receptors genes in thyroid gland","volume":"67","author":"Kajdaniuk D","year":"2016","unstructured":"Kajdaniuk D, , Marek A, , Marek B, et al. 2016. Transcriptional activity of TGFbeta1 and its receptors genes in thyroid gland. Endokrynol Pol, 67:375\u2013382.","journal-title":"Endokrynol Pol"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.imlet.2012.05.008"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2006.10.132"},{"key":"e_1_3_3_16_2","author":"Wang Y","unstructured":"Wang Y, , Zhong YJ, , Wang YY, et al. 2016 All-trans retinoic acid prevents the development of type 1 diabetes by affecting the levels of interferon gamma and interleukin 4 in streptozotocin-induced murine diabetes model. 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