Abstract：
BACKGROUND: Oral lichen planus (OLP) is a common T cell-mediated oral mucosal immune inflammatory disease. Intraepithelial lymphocytes (IELs) are a unique subset of T cells that play an important role in regulating immune response. This study aims to investigate the phenotype and the differentiation mechanism of IELs in OLP.
METHODS: The expression of CD4, CD8α, CD8β, T-helper-inducing POZ/Krueppel-like factor (ThPOK), and RUNX family transcription factor 3 (Runx3) in the epithelium and peripheral blood mononuclear cells (PBMCs) of OLP was determined by immunofluorescence and immunohistochemistry. Then, the correlations among them were analyzed. Naïve CD4+ T cells were sorted from blood of OLP patients and stimulated with retinoic acid (RA) and transforming growth factor-β1 (TGF-β1). Then the expression of CD4, CD8α, CD8β, ThPOK, and Runx3 was investigated by immunocytochemistry.
RESULTS: CD8α expression and CD8αα+ cells were upregulated in the epithelium of OLP, whereas they were downregulated in PBMCs of OLP. CD8β was not expressed in the epithelium of OLP. CD4, CD8α, and Runx3 expression and CD4+CD8α+ cells were increased, whereas ThPOK expression was decreased in the epithelium of OLP. CD8α expression was positively correlated with Runx3 expression, whereas ThPOK expression was negatively correlated with Runx3 expression. After RA and TGF-β1 stimulation, CD8α and Runx3 expression was upregulated, and ThPOK expression was downregulated in naïve CD4+ T cells.
CONCLUSIONS: CD4+CD8αα+ IELs may be the dominant phenotype of IELs in OLP, and the differentiation of CD4+CD8αα+ IELs in OLP is negatively regulated by ThPOK and positively regulated by Runx3.
METHODS: The expression of CD4, CD8α, CD8β, T-helper-inducing POZ/Krueppel-like factor (ThPOK), and RUNX family transcription factor 3 (Runx3) in the epithelium and peripheral blood mononuclear cells (PBMCs) of OLP was determined by immunofluorescence and immunohistochemistry. Then, the correlations among them were analyzed. Naïve CD4+ T cells were sorted from blood of OLP patients and stimulated with retinoic acid (RA) and transforming growth factor-β1 (TGF-β1). Then the expression of CD4, CD8α, CD8β, ThPOK, and Runx3 was investigated by immunocytochemistry.
RESULTS: CD8α expression and CD8αα+ cells were upregulated in the epithelium of OLP, whereas they were downregulated in PBMCs of OLP. CD8β was not expressed in the epithelium of OLP. CD4, CD8α, and Runx3 expression and CD4+CD8α+ cells were increased, whereas ThPOK expression was decreased in the epithelium of OLP. CD8α expression was positively correlated with Runx3 expression, whereas ThPOK expression was negatively correlated with Runx3 expression. After RA and TGF-β1 stimulation, CD8α and Runx3 expression was upregulated, and ThPOK expression was downregulated in naïve CD4+ T cells.
CONCLUSIONS: CD4+CD8αα+ IELs may be the dominant phenotype of IELs in OLP, and the differentiation of CD4+CD8αα+ IELs in OLP is negatively regulated by ThPOK and positively regulated by Runx3.
摘要：
背景：口腔扁平苔藓（OLP）是一种常见的T细胞介导的口腔黏膜免疫性炎症性疾病。上皮内淋巴细胞（IEL）是T细胞的独特亚群，在调节免疫应答中起重要作用。本研究旨在探讨OLP中IELs的表型及分化机制。
方法：CD4、CD8α、CD8β,T辅助诱导POZ/Krueppel样因子（ThPOK），通过免疫荧光和免疫组织化学测定OLP的上皮和外周血单个核细胞（PBMC）中的RUNX家族转录因子3（Runx3）。然后，分析了它们之间的相关性。从OLP患者的血液中分选初始CD4T细胞，并用视黄酸（RA）和转化生长因子-β1（TGF-β1）刺激。然后CD4、CD8α的表达，CD8β,ThPOK,通过免疫细胞化学研究Runx3。
结果：OLP上皮中CD8α表达和CD8α+细胞表达上调，而它们在OLP的PBMC中下调。CD8β在OLP上皮中不表达。CD4，CD8α，和Runx3表达和CD4+CD8α+细胞增加，而ThPOK在OLP上皮中的表达降低。CD8α表达与Runx3表达呈正相关,而ThPOK表达与Runx3表达呈负相关。在RA和TGF-β1刺激后，CD8α和Runx3表达上调，和ThPOK表达在初始CD4+T细胞中下调。
结论：CD4+CD8α+IELs可能是OLP中IELs的优势表型,OLP中CD4+CD8αα+IELs的分化受ThPOK负调控，受Runx3正调控。
方法：CD4、CD8α、CD8β,T辅助诱导POZ/Krueppel样因子（ThPOK），通过免疫荧光和免疫组织化学测定OLP的上皮和外周血单个核细胞（PBMC）中的RUNX家族转录因子3（Runx3）。然后，分析了它们之间的相关性。从OLP患者的血液中分选初始CD4T细胞，并用视黄酸（RA）和转化生长因子-β1（TGF-β1）刺激。然后CD4、CD8α的表达，CD8β,ThPOK,通过免疫细胞化学研究Runx3。
结果：OLP上皮中CD8α表达和CD8α+细胞表达上调，而它们在OLP的PBMC中下调。CD8β在OLP上皮中不表达。CD4，CD8α，和Runx3表达和CD4+CD8α+细胞增加，而ThPOK在OLP上皮中的表达降低。CD8α表达与Runx3表达呈正相关,而ThPOK表达与Runx3表达呈负相关。在RA和TGF-β1刺激后，CD8α和Runx3表达上调，和ThPOK表达在初始CD4+T细胞中下调。
结论：CD4+CD8α+IELs可能是OLP中IELs的优势表型,OLP中CD4+CD8αα+IELs的分化受ThPOK负调控，受Runx3正调控。
