Analysis dendritic cells and mucosal epithelium in oral lichen planus

口腔扁平苔藓病因不明，治疗困难。病变组织学表现为粘膜上皮基底细胞层正下方有带状T细胞浸润，基底细胞层内有Killer T细胞浸润，其浸润机制尚不清楚。我们建立了一种口腔黏膜延迟型增生的小鼠实验模型，以模拟口腔扁平苔藓。在本研究中，我们评估了参与OLP病变发展的细胞和细胞因子，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。asialo GM1抗体治疗小鼠NK细胞缺失后，由于淋巴细胞募集数量减少，DTH反应的严重程度明显降低。IL-2和INF-γ是参与病变细胞浸润的主要细胞因子。IL-2在早期病变过程中的标准表达。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。DC也可能是控制OLP的重要细胞元素。我们进一步检测了环氧化酶2 （COX2）和磷脂酶A2在OLP病变中的表达，这与口腔黏膜的特征性白色外观有关。COX2过表达与上皮细胞的厚度和棘细胞的数量呈平行关系。明确发现在上皮细胞基底细胞和巨噬细胞中存在亚群特异性PLA2、PLA2- v和PLA2- x，但不存在PLA2- iia。结果表明，在上皮细胞受到CD8阳性细胞和NK细胞损伤后，前列腺素E2等类前列腺素对上皮细胞的修复起作用。病变中COX2过表达可能与OLP的恶性转化有关。

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.