调节性T细胞（Treg）是一类具有免疫抑制功能的T淋巴细胞亚群，它在维持免疫系统自稳、调节机体免疫应答中发挥着重要的功能。研究显示其能促进肿瘤的进展及免疫逃逸，并且多种肿瘤相关因子与Treg细胞的分化及功能相关，然而关键作用分子及其机制仍未阐明。我们课题组在前期实验中应用噬菌体展示文库技术从结肠癌筛选了一系列可与na?ve CD4+T细胞结合的候选分子并对其进行了功能确认。结果显示：1、巨噬细胞抑制性细胞因子1（MIC-1）与na?ve CD4+T呈现了高亲和性；2、MIC-1表达水平与结肠癌患者TNM分期呈正相关；3、MIC-1能诱导na?ve CD4+T细胞向iTreg转化。上述结果提示MIC-1在Treg分化及结肠癌的免疫逃逸中可能发挥重要作用，那么其如何发挥诱导分化功能，具体分子机制又是什么？对上述问题的回答将为Treg分化提供新的机制，为结肠癌的肿瘤免疫治疗提供新的靶点。

T regulatory cell (Treg) is a constitutively immunosuppressive T cell type contributing to the maintenance of immunological self-tolerance and immune homeostasis. Treg cells have the ability to promote tumor progress and accelerate immune escape. It was reported that multiple molecular derived from tumor involved in Tregs differentiation and function, but the key molecular is still unclear. We screened human colon tumor T7 phage cDNA library for proteins derived from colonic cancer cells that potentially interacted with na?ve CD4+T cells. Our results revealed that, 1. MIC-1 showed high affinity with na?ve CD4+T cells. 2. MIC-1 expression level was closely correlated with the TNM stages of colon cancer patients. 3. MIC-1 could induce na?ve CD4+T cells differentiate to iTregs. The results above demonstrated that MIC-1 may play an important role in Tregs induction and immune escape process of colon cancer. Through what means did MIC-1 induced iTreg differentiation and what is the exact molecular mechanism? Answering above questions will find the new mechanism for Treg differentiation and the new immunotherapy target for colon cancer.