Please use this identifier to cite or link to this item: https://saber.ucv.ve/jspui/handle/10872/12715
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dc.contributor.authorVillarroel Dorrego, Mariana-
dc.contributor.authorCorrenti, María-
dc.contributor.authorDelgado, Rafael-
dc.contributor.authorTapia, Félix J.-
dc.date.accessioned2015-11-12T19:26:08Z-
dc.date.available2015-11-12T19:26:08Z-
dc.date.issued2002-
dc.identifier.issn0904-2512-
dc.identifier.urihttp://hdl.handle.net/10872/12715-
dc.description.abstractBackground: Current evidence suggests that immunological mechanisms are involved in oral lichen planus (OLP) pathogenesis. The events implicate activated epithelia that comprise antigen-presenting Langerhans cells, immunocompetent keratinocytes and subepithelial inflammatory infiltrate. Also, the presence of a high density of leucocyte cells may occur for the expression of a variety of adhesion molecules. The aim of this study was to analyse the immunoexpression of some adhesion molecules as well as lymphocytic markers in order to determine the disease pathogenesis in a Venezuelan population. Methods: The 18 OLP and 10 normal oral mucosa biopsies were immunostained for CD4, CD8, CD1a, LFA-1, VCAM-1 and ICAM-1. Results: The results showed an increased number of CD4þ, CD8þ, CD1aþ cells in OLP. Serial sections showed CD4þ and CD8þ cells also expressed LFA-1. The expression of ICAM-1 and VCAM-1 were significantly higher in OLP. Conclusions: The immunological reaction begins with Langerhans cells activation, which presents an antigen to CD4þ lymphocytes. Those cells through ICAM-1 and LFA-1 promote epithelial destruction. Afterwards, cytokine production, ICAM-1 and VCAM-1 expression can activate CD8þ lymphocytes leading to the chronic form of the disease.es_VE
dc.language.isoenes_VE
dc.publisherJ Oral Pathol Medes_VE
dc.relation.ispartofseries;31-
dc.subjectadhesion moleculeses_VE
dc.subjectdendritic cellses_VE
dc.subjectoral lichen planuses_VE
dc.subjectoral mucosaes_VE
dc.subjectT-lymphocyteses_VE
dc.titleOral lichen planus: immunohistology of mucosal lesionses_VE
dc.typeArticlees_VE
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