调节性T细胞（Tregs）可以促使肿瘤细胞发生免疫逃逸。结肠癌患者体内Tregs增多，但是增多的机制仍不明确。研究表明肿瘤细胞分泌的外泌体可以促使T细胞向Tregs分化。miRNA是外泌体运载的重要成分，并且已经证实某些miRNA与Tregs的生成密切相关。我们前期研究发现循环miR-208b可能是转移性结肠癌患者免疫逃逸的重要调节因子，进一步分析发现结肠癌外泌体可以运载miR-208b进入CD4+T淋巴细胞，诱导CD4+T淋巴细胞向CD25+Foxp3+T淋巴细胞分化。靶点预测与验证实验初步证实T淋巴细胞中的PDCD4基因为miR-208b的靶基因。本研究旨在原有研究的基础上，进一步验证结肠癌外泌体中的miR-208b能否诱导Tregs生成促使肿瘤免疫逃逸，并探讨PDCD4基因在这一过程中的作用。这对解释结肠癌免疫逃逸的机制有重要的意义，更为结肠癌靶向治疗提供新的方向和靶点。

Tumors have the capacity to escape from immune surveillance by numerous mechanisms. One of which is an increase in the population of regulatory T cells (Tregs). Tregs are increased during tumor progression in colon cancer, but the precise mechanism remains poorly understood. Studies indicated that exosomes derived from tumor cells can promote the differentiation of T cells to Tregs, and miRNAs which are key components in the exosomes are important for the maintenance of Tregs homeostasis. In our previous studies, miR-208b was found to be probably related with the immune evasion of colon cancer patients. We also found that miR-208b was sufficiently delivered into CD4+T cells and the percentage of CD25+Foxp3+T cells was obviously increased when CD4+T cells was incubated with SW-480-derived exosomes together. Target prediction and validation assay indicated that PDCD4 was the target gene of miR-208b. In this proposal, we will further verify whether exosome-delivered miR-208b regulates the differentiation of Tregs to promote colon cancer immune evasion. We will also explore the important role of PDCD4 gene in this process. Our study will not only reveal a novel mechanism of immune evasion in colon cancer, but also provide a new direction and a target for colon cancer targeting therapy.