The cellular character of liquefaction degeneration in oral lichen planus and the role of Interferon gamma

Abstract

Background

Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology, liquefaction degeneration in the basal keratinocytes is one of the specific histological changes. However, the understanding of liquefaction degeneration is still very limited, and how does it affect the prognosis of LP is largely unknown. Therefore, the objective of this study is to clarify the intrinsic change behind the liquefaction degeneration in lichen planus, and evaluate the effect of the OLP typical cytokines IFN-γon these changes.

Materials And Methods

Biopsies were collected from OLP patients, immunochemistry staining was performed to analysed E-cadherin, vimentin, CK19, β1 integrin, nestin, STAT1 and STAT3 expression. Primary oral epithelial cells were cultured in vitro, 20ng/ml IFN-γwas applied to assay the effect on epithelial cells.

Results

E-cadherin expression was decreased but vimentin expression was increased in the OLP epithelial cells undergo liquefaction degeneration, showing the typical epithelial-mesenchymal transition (EMT) alteration. In vitro research showed that OLP typical cytokine, IFN-γpossesses EMT inducing ability, and the primary oral epithelial cells stimulated by IFN-γacquired some properties of cancer stem cells, expressing moreβ1 integrin,α6 integrin and nestin. In addition, the major downstream mediator of IFN-γreceptors, STAT1 was expressed more intensive and extensive with the malignant transition of OLP.

Conclusion

Liquefaction degeneration in oral lichen planus is an EMT phenomenon, the IFN-γ may be the main inducer, and IFN-γsignaling might be implicated in malignant transition of OLP.

This article is protected by copyright. All rights reserved.

from #Medicine-SfakianakisAlexandros via o.lakala70 on Inoreader http://ift.tt/2s6AfBg
via IFTTT Medicine by Alexandros G.Sfakianakis,Anapafseos 5 Agios Nikolaos,Crete 72100,Greece,tel :00302841026182 & 00306932607174

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