髓系抑制性细胞(MDSC)通过抑制T细胞促进肿瘤免疫逃逸，导致肿瘤的发生发展。我们前期研究发现甲状腺乳头状癌(PTC)患者MDSC (CD11b+CD14-CD33+)比例明显升高，MDSC显著抑制CD4+T细胞增殖。进一步研究发现miR-181b 和PD-L1在PTC患者的MDSC中表达明显升高。我们推测miR-181b可能靶向作用于PTEN，通过ATK通路增加mTOR的信号活性而上调MDSC中PD-L1的水平，在MDSC介导的肿瘤免疫逃逸中扮演重要角色。本研究拟采用细胞模型、动物模型及分子生物学实验探明MDSC中表达升高的miR-181b通过PTEN-ATK-mTOR-PD-L1通路调控T细胞的作用；与临床样本数据相结合，进一步验证 MDSC通过miR-181b调控PD-L1的表达对T细胞的负调控作用，为PTC的免疫治疗提供新方向及手段。

Myeloid-derived Suppressor Cells (MDSC) promote immune escape in tumor occurrence and development by inhibiting T cell activation. Our preliminary data determined that MDSC (CD11b+CD14-CD33+) were significantly increased in patients with papillary thyroid carcinoma (PTC.), and showed that MDSC from patients inhibited CD4+ T cell proliferation. Further study found that the expression of miR-181b an PD-L1were significantly increased in MDSC of the patient with PTC, which might be involved in the development and invasion of PTC through promoting immune escape. We hypothesized that miR-181b may down regulate immune response through ATK signal pathways by target on PTEN, and then increased the activity of mTOR and raised the level of PD-L1. In this project, we will use in vitro and in vivo experiments to study the roles of miR-181b upregulated in MDSC in PTC immune escape and the underlining mechanisms. By combining with clinical data, we are trying to verify that MDSC down regulate immune response through the expression of PD-L1 regulated by miR-181b, providing new treatment targets for PTC.