T细胞异常迁徙与募集是OLP发病中重要事件，然而，固有层T淋巴细胞异常密集的机理仍不清楚。趋化因子是一类能趋化细胞定向移动的细胞因子，通过受体诱导细胞定向迁移，并影响其他细胞因子分泌，在维持体内免疫平衡中发挥重要作用，课题组前期研究发现：OLP存在Th1/Th2失衡，部分趋化因子受体与调控OLP发病机制的免疫相关蛋白的异常表达密切相关。本课题拟通过病损和外周血确定CCR1、CCR4、CCR8、CCR9、CXCR3等趋化因子受体在OLP与健康成人中表达的差异，探讨其与OLP患者Th1/Th2失衡的关系，并通过体外淋巴细胞培养、基因沉默技术，寻找Cytokine-cytokine receptor interaction cc subfamily通路关键信号分子，探讨其对外周血T细胞及口腔黏膜角质形成细胞的生物学行为及炎症效应产生的影响，意在阐明OLP免疫发病机制，为临床治疗提新靶点。

The abnormal migration and recruitment of T lymphocytes play a key role in the pathogenesis of oral lichen planus.However,the mechanism of subepithelial inflammatory infiltrate consisting predominantly of T lymphocytes remains unclear.Chemokines represent a family of small cytokines or proteins,which direct the cellular migration by interacting with specific receptors and influence the secretion of other cytokines. They play a crucial role in maintaining immune balance.Our recent studies show that patients with OLP have an imbalance of Th1/Th2 and partial chemokine receptors are closely related with the expression of a certain immunological protein which participates in the pathogenesis of oral lichen planus. We plan to study the expression of CCR1、CCR4、CCR8、CCR9、CXCR3 in patients with oral lichen planus and healthy adults,exploring its linkage with the imbalance of Th1/Th2 in patients with oral lichen planus. we also expect to find the key signal molecule of the cytokine-cytokine receptor interaction cc subfamily pathway through gene interference,approaching its influence towards T lymphocytes and oral keratinocytes.We hope all the researches above can elucidate the pathogenesis of oral lichen planus and provide new molecular targets for therapy.