{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T04:36:08Z","timestamp":1785386168992,"version":"3.55.0"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,4,12]],"date-time":"2015-04-12T00:00:00Z","timestamp":1428796800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008247","name":"University of Otago","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008247","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Oral Pathology Medicine"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>The objective of this study was to investigate the expression of Toll\u2010like receptors (TLR) and TLR\u2010associated signalling pathway genes in oral lichen planus (OLP).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Initially, immunohistochemistry was used to determine TLR expression in 12 formalin\u2010fixed archival OLP tissues with 12 non\u2010specifically inflamed oral tissues as controls. RNA was isolated from further fresh samples of OLP and non\u2010specifically inflamed oral tissue controls (<jats:italic>n<\/jats:italic>\u00a0=\u00a06 for both groups) and used in qRT<jats:sup>2<\/jats:sup>\u2010PCR focused arrays to determine the expression of TLRs and associated signalling pathway genes. Genes with a statistical significance of \u00b1two\u2010fold regulation (FR) and a <jats:italic>P<\/jats:italic>\u2010value\u00a0&lt;\u00a00.05 were considered as significantly regulated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Significantly more TLR4<jats:sup>+<\/jats:sup> cells were present in the inflammatory infiltrate in OLP compared with the control tissues (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). There was no statistically significant difference in the numbers of TLR2<jats:sup>+<\/jats:sup> and TLR8<jats:sup>+<\/jats:sup> cells between the groups. TLR3 was significantly downregulated in OLP (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01). TLR8 was upregulated in OLP, but the difference between the groups was not statistically significant. The TLR\u2010mediated signalling\u2010associated protein genes MyD88 and TIRAP were significantly downregulated (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01 and <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), as were IRAK1 (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), MAPK8 (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01), MAP3K1 (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), MAP4K4 (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), REL (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01) and RELA (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01). Stress proteins HMGB1 and the heat shock protein D1 were significantly downregulated in OLP (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings suggest a downregulation of TLR\u2010mediated signalling pathways in OLP lesions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jop.12319","type":"journal-article","created":{"date-parts":[[2015,4,13]],"date-time":"2015-04-13T04:26:49Z","timestamp":1428899209000},"page":"28-34","source":"Crossref","is-referenced-by-count":18,"title":["Downregulation of toll\u2010like receptor\u2010mediated signalling pathways in oral lichen planus"],"prefix":"10.1111","volume":"45","author":[{"given":"Suraya H.","family":"Sinon","sequence":"first","affiliation":[{"name":"Department of Oral Pathology and Oral Medicine Faculty of Dentistry Universiti Kebangsaan Malaysia (UKM) Kuala Lumpur Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison M.","family":"Rich","sequence":"additional","affiliation":[{"name":"The Sir John Walsh Research Institute Faculty of Dentistry University of Otago Dunedin New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Venkata P. 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