microRNAs在免疫调节过程中发挥了重要功能，LPS能够下调巨噬细胞中miR-34a的表达；趋化因子CCL22是受miR-34a调控的靶分子，通过招募Treg细胞发挥免疫调节功能。Treg细胞在根尖周炎的病理过程中发挥了重要作用，但是，Treg细胞在根尖周病损中被募集的机制仍不清楚。本研究将探讨miR-34a-CCL22信号轴是否参与了根尖周炎中Treg细胞的招募及其效应。本项目主要研究内容包括：① miR-34a是否参与LPS对巨噬细胞CCL22表达的调控；② 抑制miR-34a后，阻断CCL22对Treg细胞迁移的影响；③ 在大鼠实验性根尖周炎的不同阶段，观察miR-34a和CCL22表达水平的变化，Treg细胞数量的变化及其与破骨细胞数量、根尖周病损大小的效应关系。通过本项目的研究，可以加深我们对根尖周炎病理过程的认识，并为根尖周炎的防治提供新的思路。

Accumulating evidence has identified microRNAs as critical regulators in immune responses such as release of inflammatory mediators. Macrophages respond quickly to pathogen components, such as LPS from the outer membrane of Gram-negative bacteria and miR-34a is down-regulated by LPS in macrophages. CCL22, one of targets of miR-34a, binds to its receptor CCR4 on the surface of Treg cells, consequently recruiting those immunosuppressive cells to the microenvironment for immune surveillance. Previous studies reported that Treg cells play important roles in the pathogenesis of periapical lesions. However, the molecular mechanisms involved in the recruitment of Treg cells in periapical lesions remains elusive. The aim of present study was to investigate the potential role of LPS-miR-34a-CCL22 signaling in recruiting Treg cells in periapical lesions and the relationship between Treg cells and osteoclasts and inflammatory responses. The research proposals include: ① Whether LPS modulates the expression of CCL22 via miR-34a; ② The effect of blocking CCL22 on the migration of Treg cells after inhibiting miR-34a; ③ At different stages of rat periapical lesions, the levels of miR-34a and CCL22 will be detected and the relationship between number of Treg cells and periapical bone resorption will also be analysed. The study of present project facilitates our better understanding of the pathogenesis of periapical lesions and reveals new targets for treatment of periapical lesions.