肺癌细胞促进调节性T细胞表面分子GARP（LRRC32）表达及其机制研究

肿瘤微环境中的CD4+CD25+调节性T细胞群（Tregs）可以通过抑制机体的免疫反应，从而促进肿瘤的生长和转移。研究显示活化的Tregs细胞表面分子GARP蛋白能够结合细胞因子TGF-beta，从而在Tregs细胞表面形成GARP-mbTGF-beta复合物，而该复合物则参与了Tregs细胞的免疫抑制作用。本研究希望通过检测肺癌组织中GARP+Tregs细胞数量和TGF-beta表达及空间分布，并结合临床病理资料，分析GARP+的Tregs细胞与肿瘤的进展和转移是否具有更好的相关性。此外希望通过研究肿瘤细胞促进表面分子GARP蛋白的表达进而活化Tregs细胞的机制，以期探讨肿瘤免疫抑制的新途径：肿瘤微环境中的肿瘤细胞能够促进Tregs细胞表面分子GARP的表达，从而增强肿瘤局部免疫抑制能力，促进肿瘤的发展和转移。

CD4+CD25+ regulatory T cells (Tregs) can suppress the body`s immune response in the tumor microenviroment to promote the development and metastasis of tumor. The membrane protein GARP expressed in the activated Tregs can bind the cell growth factor TGF-beta and form a large complex GARP-mbTGF-beta which is thought to participate in the immune suppression of Tregs. In this research, the amount of GARP+Tregs, expression and spatial distribution of TGF-beta will be assayed by immunohistochemisty in tumor specimens from lung cancer patients. The results will be analyzed to determine whether GARP+Tregs have a better correlation with tumor`s development and metastasis. To investigate the mechanism that breast cancer cells activate Tregs through increasing GARP expression in Tregs` surface, a new hypothesis about tumor immune suppression will be discussed: In tumor microenviroment, cancer cells will activate Tregs by GARP to increase the immune suppression, as a result leading the development and metastasis of tumor .