Analysis dendritic cells and mucosal epithelium in oral lichen planus

口腔扁平苔藓是一种病因不明的难治性疾病。病变的组织学特征是粘膜上皮基底细胞层下的带状T细胞浸润和基底细胞层中的杀伤T细胞浸润，但这些细胞浸润的某些机制尚不清楚。我们建立了一种模拟口腔扁平苔藓的小鼠口腔粘膜迟发性增生模型。在本研究中，我们评估了细胞和细胞因子参与OLP发展的病变，以开发有用的治疗系统。我们的结果清楚地表明NK细胞在病变的早期发展中起关键作用。去唾液酸GM 1抗体处理小鼠后NK细胞缺失，由于淋巴细胞募集数量减少，明显显示DTH反应的严重程度降低。IL-2和INF-γ是参与病变细胞浸润的主要细胞因子。IL-2在早期病变过程中标准表达。这些细胞和细胞因子调节疾病的发展。病变的另一个特征是大量树突状细胞（DC）浸润到上皮层。DC也可能是控制OLP的重要细胞因子。我们进一步检测了OLP病变的环氧化酶2（COX 2）和磷脂酶A2的表达，这与口腔粘膜上的特征性白色外观有关。COX 2的表达与上皮厚度及棘细胞数量有关。结果表明，在上皮基底细胞和巨噬细胞中，PLA 2-V和PLA 2-X是亚群特异性的，而PLA 2-IIa则不存在。结果表明，前列腺素样前列腺素E2在上皮细胞受到CD 8阳性细胞和NK细胞损伤后的修复中发挥作用。COX 2在OLP中的过度表达可能与OLP的恶变有关。

Oral lichen planus is difficult to cure with unknown etiology. The lesion is characterized histological by band-like T cells infiltration just under the basal cell layer of mucosal epithelium and Killer T cell infiltration into the basal cell layer, while certain mechanism of 'these cells infiltration were not clarified. We have developed a mouse experimental model of oral mucosal delayed type hyperplasia as a mimic of oral lichen planus. In this study, we evaluated the cells and cytokine involve OLP development the lesion for the development of useful treatment system. Our result clearly indicted that NK cell play key role for the early development of the lesion. NK cells deletion following asialo GM1 antibody treatment mouse that was clearly showed decrease the severity of DTH reaction due to the less number of lymphocytes recruitment. IL-2 and INF-γ are major cytokines involved in cell infiltration of the lesion. IL-2 revealed by standard expression at course of early lesion. These cell and cytokines regulate disease development. Another characteristic feature of the lesion is numerous dendritic cells (DC) infiltrate in to the epithelial layer. DC may also important cell elements for the controlling the OLP. We further examined cyclooxigenase 2 (COX2) and Phospholipase A2 expression of the OLP lesion, which relate to characteristic white color appearance on oral mucosa. COX2 over expression was paralleled to thickness of epithelium and amounts of prickle cells in the epithelium. Clear finding obtained that subgroup specific PLA2, PLA2-V and PLA2-X but not for PLA2-IIa, were identified in the basal cells of epithelium and macrophages. The results indicted prostanoid like prostaglandin E2 play a role for the epithelial cell repair following epithelial cells received damage by CD8 positive cell and NK cells. More over the COX2 over expression in the lesions may be related to malignant transformation of OLP.