前期研究显示Th-GM能够浸润到滑膜，诱导中心粒细胞聚集，增强骨髓及滑膜成纤维细胞（FLS）释放炎症因子，加重关节炎症。然而Th-GM如何浸润到RA患者滑膜仍不清楚。预实验结果提示RA患者滑膜高表达CCL28，以及Th-GM高表达CCR10，因此本研究提出RA滑膜表达CCL28促进Th-GM浸润到滑膜的假说，为证明该假设，我们首先在CIA模型中通过抗体阻断以及干扰技术验证RA滑膜表达CCL28促进Th-GM的浸润；其次通过Th-GM细胞移植实验结合双光子显微镜动态观察Th-GM浸润到滑膜的过程；然后将CCL28作用的Th-GM通过二代测序、DIA蛋白质组学筛选与血管细胞作用及迁移相关的通路和分子。最后通过Co-IP、CHIP等技术验证Th-GM在CCL28作用下穿过血管内皮细胞至滑膜组织的分子机制。本研究可阐明滑膜表达CCL28在RA发病过程中的机制，可以为RA治疗提供新思路。

Previous studies have shown that Th-GM cells can infiltrate into joints, inducing aggregation of central granulocytes into the synovial membrane, and enhancing the release of inflammatory factors by bone marrow and synovial fibroblasts (FLS). However, the pathologic process of Th-GM cells infiltration into the joints of RA patients remains unclear. The preliminary experimental results suggested that there is high level of CCL28 in synovial of RA patients and Th-GM cells are CCR10 positive. Therefore, we proposed a hypothesis that the synovial membrane expressed CCL28 to promote Th-GM infiltrating into synovial membrane. To prove the hypothesis, we first verified that the expression of CCL28 in the synovial membrane of RA promoted the infiltration of Th-GM cells in CIA mouse model through antibodies blocking and interference. Secondly, Th-GM cell transplantation experiment and two-photon microscope were used to observe the infiltration of Th-GM into synovium. Then screened for the pathways and molecules related to the function and migration of endothelial cells and outer membrane fibroblasts by second generation sequencing and DIA proteomics. Finally, Co-IP, CHIP and other technologies were used to verify the mechanism of Th-GM passing through vascular cells to synovial tissue under the action of CCL28. This study can clarify the mechanism of synovial expression of CCL28 in the pathogenesis of RA and provide new ideas for the treatment of RA.