Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2017
The cellular character of liquefaction degeneration in oral lichen planus and the role of interferon gamma.
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Liu Yuan, Liu Guicai, Liu Qing, Tan Jun, Hu Xin, Wang Jinjin, Wang Qintao, Wang Xinwen
Аннотация
BACKGROUND: Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology, and 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 was to clarify the intrinsic change behind the liquefaction degeneration in lichen planus and to evaluate the effect of the OLP-typical cytokine, IFN-γ, on these changes.
MATERIALS AND METHODS: Biopsies were collected from patients with OLP; immunochemistry staining was performed to analyze E-cadherin, vimentin, CK19, β1 integrin, nestin, STAT1, and STAT3 expression. Primary oral epithelial cells were cultured in vitro, and 20 ng/mL IFN-γ was applied to assay the effect on epithelial cells.
RESULTS: E-cadherin expression was decreased but vimentin expression was increased in the OLP epithelial cells that undergo liquefaction degeneration, showing the typical epithelial-mesenchymal transition (EMT) alteration. In vitro research showed that the OLP-typical cytokine, IFN-γ, possesses EMT-inducing ability, and the primary oral epithelial cells stimulated by IFN-γ acquired some properties of cancer stem cells, expressing more β1 integrin, α6 integrin, and nestin. In addition, the major downstream mediator of IFN-γ receptor, 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-γ signaling might be implicated in malignant transition of OLP.
MATERIALS AND METHODS: Biopsies were collected from patients with OLP; immunochemistry staining was performed to analyze E-cadherin, vimentin, CK19, β1 integrin, nestin, STAT1, and STAT3 expression. Primary oral epithelial cells were cultured in vitro, and 20 ng/mL IFN-γ was applied to assay the effect on epithelial cells.
RESULTS: E-cadherin expression was decreased but vimentin expression was increased in the OLP epithelial cells that undergo liquefaction degeneration, showing the typical epithelial-mesenchymal transition (EMT) alteration. In vitro research showed that the OLP-typical cytokine, IFN-γ, possesses EMT-inducing ability, and the primary oral epithelial cells stimulated by IFN-γ acquired some properties of cancer stem cells, expressing more β1 integrin, α6 integrin, and nestin. In addition, the major downstream mediator of IFN-γ receptor, 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-γ signaling might be implicated in malignant transition of OLP.