口腔扁平苔藓发病机制中T细胞和肥大细胞的作用

口腔扁平苔藓(OLP)是一种T细胞介导的较为常见的慢性口腔粘膜疾病,其发病机制可能包括抗原特异性和非特异性两种。本文就OLP发病机制中T细胞与肥大细胞的作用作一综述。     

口腔扁平苔藓发病机制中T细胞和肥大细胞的作用

口腔扁平苔藓(OLP)是一种T细胞介导的较为常见的慢性口腔粘膜疾病，其发病机制可能包括抗原特异性和非特异性两种。本文就OLP发病机制中T细胞与肥大细胞的作用作一综述。     

口腔扁平苔藓的免疫发病机制研究进展

免疫因素在口腔扁平苔藓 (OLP)的发生、发展过程中占主要地位 ,目前认为OLP是一种细胞介导的、由外来抗原或改变的自身抗原导致的口腔黏膜基底角质细胞的免疫破坏性慢性疾病     

5-羟色胺与口腔扁平苔藓的相关性研究进展

口腔扁平苔藓(oral lichen planus, OLP)是一种慢性炎症性黏膜病，已有文献表明精神因素是其重要的致病因素之一。同时，OLP又是一种免疫失调引起的自身免疫性疾病，笔者怀疑精神因素可能通过某些因子作用于局部免疫，引起免疫失调，从而在OLP的发病机制中发挥作用。5-羟色胺(5-hydroxytryptamine, 5-HT)是一种单胺类神经递质，可作为神经系统和免疫系统双边接触的介质。5-HT可能通过与多种受体结合，激活不同信号通路，对情绪调节以及免疫细胞的增殖、迁移、凋亡等过程均起到重要的调节作用。近年来的研究表明5-HT可能参与OLP的发生、发展过程。该文针对5-HT及其受体的功能、它们在自身免疫性疾病中的特异性表达以及在OLP中可能发挥的作用作一综述。     

口腔扁平苔藓中树突状细胞的研究现状

口腔扁平苔藓（OLP）是口腔黏膜疾病中具有代表性的一种自身免疫性疾病,其病因依然不明确,自身抗原的异常表达和识别被认为可能是引发疾病的一大原因。树突状细胞是抗原提呈能力最强的细胞,是激活T细胞免疫的主要途径。在OLP中,树突状细胞的数量明显增加,其类型也与正常黏膜组织中有所差异;其趋化因子受体的表达表现出活化的功能状态;其识别抗原的Toll样受体在OLP组织中也有明显的差异表达。本文就树突状细胞在OLP中的亚群／生物标记物、趋化因子表达、Toll样受体表达等方向的研究现状做一综述。     

口腔扁平苔藓的特异性免疫机制研究进展

口腔扁平苔藓的发生与机体的免疫机制密切相关,特异性免疫机制尤为重要.特异性免疫主要是指基底角质细胞表达相关抗原和CD8+细胞毒性T细胞杀伤抗原特异性角质细胞,并在过程中释放相应的细胞因子引起黏膜的损伤.本文综述了口腔扁平苔藓与特异性免疫机制之间的关系,展示其研究现状和前景.     

口腔扁平苔藓的精神发病因素与神经免疫的研究进展

口腔扁平苔藓(OLP)存在多种发病机制假说,其中精神因素发病机制认为,精神因素可以通过应激轴引起神经免疫反应导致OLP的发生,本文就对精神因素以及神经免疫与OLP的关系等研究进展作一综述。     

口腔扁平苔藓会传染吗？

口腔扁平苔藓（OLP）是一种可能与多种致病因素有关的口腔黏膜慢性炎性疾病，研究发现OLP的发生发展可能与细菌、病毒、真菌等感染因素有关，因此，有关OLP是否会传染的问题受到临床医师及患者的关注。本文分析总结了可能与OLP密切相关的感染因素，提出OLP可能会传染的观点。     

聚肌胞注射液治疗口腔扁平苔藓的短期疗效观察

口腔扁平苔藓(OLP)是口腔黏膜常见的非感染性疾病，近年来的研究表明，OLP可能是一种局限性的自身免疫性疾病。OLP尚无特效疗法，研究发现氯喹治疗OLP有显著疗效，但因长期服用有明显毒副作用，使其临床应用受到限制。本研究观察聚肌胞注射液局部封闭口服氯喹两种方法治疗糜烂型OLP有一定临床疗效，现报道如下：     

精神因素与口腔扁平苔藓的相关性研究进展

口腔扁平苔藓(oral lichen planus,OLP)是发生在口腔黏膜的一种慢性炎症性疾病,好发于中年人,女性发病率略高于男性[1].病因尚不明确,可能的致病因素包括感染、免疫功能紊乱以及精神因素等.近年来随着现代心身医学研究的发展,OLP的精神病因学说日益受到研究者更多的关注,现对该方面的研究进行回顾性总结.     

Immune mechanisms in oral lichen planus

Oral lichen planus (OLP) is a T cell-mediated inflammatory disease of the oral mucosa that has been extensively researched over many years but as yet the mechanisms of pathogenesis are still not fully understood. Whilst the specific aetiological factors driving OLP remain ambiguous, evidence points to the development of a chronic, dysregulated immune response to OLP-mediating antigens presented by innate immune cells and oral keratinocytes leading to increased cytokine, chemokine and adhesion molecule expression. These molecules recruit T cells and mast cells to the diseased site and orchestrate a complex interplay between cells that culminates in keratinocyte cell death, mucosal basement membrane destruction and long-term chronicity of the disease. The main lymphocytes involved are thought to be CD8+ cytotoxic and CD4+ Th1 polarised T cells although recent evidence indicates the involvement of other Th subsets such as Th9, Th17 and Tregs, suggesting that a more complex immune cell relationship exists during the disease process. This review provides an overview of the immune mechanisms at play in OLP pathogenesis with particular emphasis on the role of the different Th subsets and how these recent discoveries may guide research towards identifying potential therapeutic targets.     

Mast cell/T cell interactions in oral lichen planus

Lichen planus is a disorder characterized by lesions of the skin and oral mucous membranes. Although many patients have involvement of both skin and oral mucosa at some stage during the progress of the disease, a larger group has oral involvement alone. It has been reported that oral lichen planus (OLP) affects one to two percent of the general population and has the potential for malignant transformation in some cases (1, 2). Like many chronic inflammatory skin diseases, it often persists for many years. Numerous disorders may be associated with OLP such as graft-vs.-host disease and Hepatitis C virus infection (3), however, it is unclear how such diverse influences elicit the disease and indeed whether they are identical to idiopathic OLP. Available evidence supports the view that OLP is a cell-mediated immunological response to an induced antigenic change in the mucosa (4-6). Studies of the immunopathogenesis of OLP aim to provide specific novel treatments as well as contributing to our understanding of other cell-mediated inflammatory diseases. In this paper, the interactions between mast cells and T cells are explored from the standpoint of immune regulation. From these data, a unifying hypothesis for the immunopathogenesis of OLP is then developed and presented.     

转录因子RORγτ和FOXP3在口腔扁平苔藓病损组织中的表达及意义

目的:口腔扁平苔藓(oral lichen planus,OLP)是一种发生于口腔黏膜的T淋巴细胞介导的自身免疫性疾病。辅助性T细胞(helper T lymphocytes, Th)在OLP的发病过程中具有重要作用,本研究旨在进一步探索OLP患者局部病损组织中辅助性T细胞亚群Th17细胞和Treg细胞的作用。方法:纳入43例OLP患者和13例健康志愿者。采用实时定量PCR法检测局部病损组织中Th17和Treg细胞的特征性转录因子RORγτ和FOXP3的表达,采用GraphPad Prism 5 软件对其表达差异进行统计学分析。结果:OLP局部病损组织中转录因子RORγτ和FOXP3的表达显著高于正常黏膜组织,而且均与OLP的临床分型密切相关。萎缩糜烂型OLP组病损组织中RORγτ/FOXP3比值显著高于网状型OLP组和健康对照组,而网状型OLP组的RORγτ/FOXP3比值虽然高于对照组,但差异无显著性。结论:Th17细胞和Treg细胞均参与OLP的局部免疫反应;同时,Th17/Treg失衡也参与了重症型OLP的致病过程,且表现为Th17细胞优势。     

Oral lichen planus. A review

Lichen planus is a mucocutaneous disease of unknown etiology which, according to current knowledge, may represent a cell-mediated immunological response to induced antigenic changes in the skin and mucosa. Oral lichen planus (OLP) is a disease of adulthood and as one of the most prevalent diseases affecting the oral mucosa it has been the subject of intensive research during recent years. Ultrastructural and immunohistochemical studies particularly dealing with the subepithelial inflammatory cell infiltrate and its relations to epithelial pathology, the basal cell region and the intraepithelial antigen presenting Langerhans' cells, have contributed vastly to our knowledge of the pathogenesis of OLP. However, the treatment of OLP still remains largely symptomatic because many as yet unknown factors, active in the disease process, still remain to be elucidated.     

人β防御素2与口腔扁平苔藓相关性的研究进展

口腔扁平苔藓(oral lichen planus,OLP)是一种常见的口腔黏膜慢性免疫性炎症疾病,OLP的病因和发病机理目前尚未阐明,在临床诊疗过程中存在着诸多问题且OLP存在癌变风险,故OLP的发生发展及临床诊疗方面的研究历来受到重视.近年来的一些研究表明,OLP的发生与人β防御素2(humanβdefensin-...     

Immunohistopathological study of the oral lichenoid lesions of chronic GVHD

BACKGROUND: Chronic graft-vs.-host disease (cGVHD) is a common and serious complication after bone marrow transplantation (BMT). However, the detailed process of oral lichenoid lesions of cGVHD is still unknown. Therefore, we investigated the immunohistopathological features of cGVHD compared with oral lichen planus (OLP) and healthy controls. METHODS: Nineteen allogenic BMT recipients with a histopathological diagnosis of cGVHD were investigated. We investigated the immunohistopathological features of cGVHD compared with OLP and healthy controls. RESULTS: Immunohistopathological features showed that the infiltrations of CD4-positive T cells of cGVHD and OLP were significantly larger than those of the normal oral mucosa (P < 0.005). A larger number of CD8-positive T cells was infiltrated in cGVHD and OLP compared with the normal oral mucosa (P < 0.001). The difference in the number of CD4- and CD8-positive T cells between cGVHD and OLP was not significant. The infiltrations of Langerhans cells (CD1a) in cGVHD and OLP were significantly larger than those in the normal oral mucosa (P < 0.005). The difference in the number of Langerhans cells between cGVHD and OLP was not significant. CD68-positive macrophages were more frequently seen in cGVHD and OLP than in the normal oral mucosa (P < 0.0001). The difference in the number of CD68-positive macrophages between cGVHD and OLP was not significant. CONCLUSIONS: It is suggested that Langerhans cells and CD8-positive T cell may play a major role in the pathogenesis of the oral lichenoid lesions of cGVHD, and the immune response was inducted in OLP as well as the oral lichenoid lesion of cGVHD in this study.     

凋亡蛋白Bcl-2、Bax在白斑、口腔扁平苔藓中的表达

目的:观察凋亡蛋白Bcl-2、Bax在白斑、口腔扁平苔藓上皮细胞中的表达,探讨其在口腔白斑、口腔扁平苔藓癌变过程中的作用机制。方法:采用免疫组化法检测10例正常口腔黏膜上皮、18例口腔扁平苔藓、23例白斑、22例口腔鳞癌上皮组织中凋亡相关蛋白Bcl-2、Bax的表达水平。结果:Bcl-2在白斑、口腔扁平苔藓上皮细胞层无异常表达,但在口腔扁平苔藓淋巴细胞浸润带过度表达。Bcl-2在鳞癌组织中呈高表达,与正常黏膜相比有显著性差异(P<0.05)。Bax在上皮单纯增生、轻度、中度不典型增生和低分化鳞癌及糜烂型口腔扁平苔藓组织中呈过度表达,与正常黏膜相比有显著性差异(P<0.05)。结论:Bax参与了口腔白斑癌变的早期事件,而Bcl-2在不典型增生转化为鳞癌的阶段并未发生作用。口腔扁平苔藓的发病机制可能与Bcl-2抑制淋巴细胞凋亡,使细胞免疫亢进,从而刺激上皮细胞Bax过度表达,诱导角朊细胞凋亡有关。     

口腔扁平苔藓固有层淋巴细胞中Fas及Fas配体的表达变化

目的 检测Fas及Fas配体(Fas ligand,FasL)在口腔扁平苔藓(oral lichen planus,OLP)固有层淋巴细胞中的蛋白表达,探讨Fas、FasL和活化诱导的细胞死亡(activation-induced cell death,AICD)与OLP发病的关系.方法 采用脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记法检测31例OLP和10例正常口腔黏膜(normal oral mucosa,NOM)中淋巴细胞凋亡情况;分别使用免疫组化法检测组织总淋巴细胞及CD8~+、CD4~+T细胞Fas、FasL的表达.结果 OLP与NOM固有层淋巴细胞凋亡率[分别为(1.9±1.8)%、(11.5±9.0)%]差异有统计学意义(P=0.013).OLP淋巴细胞Fas、FasL表达与NOM组相比明显增强[阳性表达率分别为52%(16/31)、71%(22/31),P值分别为0.005、0.000].OLP中CD8~+与Fas~+细胞双阳性表达率为10%,与NOM组相比无明显升高(P=0.313),而CD8~+与FasL~+细胞双阳性表达率[58%(3/31)]显著升高(P=0.002).CD4~+与Fas~+细胞双阳性表达率为35%(11/31),较NOM组显著升高(P=0.031),其中网纹型的表达明显升高(阳性表达为8/19,P=0.019),但糜烂、萎缩型的表达无显著升高(阳性表达为3/12,P=0.097).CD4~+与FasL~+表达率为16%(5/31),与NOM组相比无明显增强(P=0.182).结论 OLP淋巴细胞凋亡低下;OLP中T细胞亚群Fas、FasL表达不均衡,CD8~+细胞和萎缩、糜烂型OLP中CD4~+细胞可能逃逸AICD,与炎症的持续和进展有关;网纹型OLP中部分CD4~+T细胞可能经历AICD.     

Role of apoptosis in erosive and reticular oral lichen planus exhibiting variable epithelial thickness

Oral lichen planus (OLP) is a chronic inflammatory disease with different clinical types. Reticular and erosive forms are the most common. Although the cause of OLP remains speculative, many findings suggest auto-immune involvement, mediated by T lymphocytes against the basal keratinocytes. Inflammation, mechanical trauma or toxic agents can affect the epithelial homeostasia. Increased apoptosis may cause a decrease in epithelial thickness reflecting in the activity of the lesion. The objective of this study was to evaluate the occurrence of apoptosis and epithelial thickness in reticular and erosive forms of OLP. 15 samples of OLP each type (reticular and erosive) plus 10 of healthy mucosa were collected and processed. After morphometry, the apoptotic index and epithelial thickness were obtained. TUNEL and M30 CytoDEATH immunohistochemical assay were used to validate the morphologic criteria used. Apoptosis in the erosive OLP was significantly more intense than in the reticular type and both forms of OLP presented more apoptosis than the healthy oral mucosa. Healthy oral mucosa was thicker than both OLP forms and thicker in OLP reticular form than in the erosive one. The clinical differences between reticular and erosive forms of OLP are related to variations in epithelial thickness and in intensity of apoptosis.