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目的探讨子宫内膜癌患者外周血及癌组织CD4+CD25+Treg细胞水平与子宫内膜癌发生发展的关系,及其在肿瘤免疫逃逸中的作用机制。方法 26例子宫内膜癌患者外周血经Ficoll梯度离心分离单个核细胞,同时取手术切除的新鲜肿瘤组织进行肿瘤浸润性淋巴细胞和非肿瘤浸润性淋巴细胞制备。应用流式细胞仪分析CD4+CD25+Treg细胞的分布比例,并与25例年龄相匹配的健康对照者的外周血CD4+CD25+Treg细胞比例为对照,并用ELISA方法检测同标本血中Treg细胞分泌的抑制性细胞因子IL-10和转化生长因子(TGF-β)水平及趋化因子受体CCR4水平。结果子宫内膜癌患者CD4+CD25+Treg细胞比例明显高于癌旁组织及对照组(P<0.05);IL-10、TGF-β水平明显高于对照组,提示Treg通过分泌IL-10和TGF-β等抑制性细胞因子及细胞接触依赖的抑制途径,抑制免疫效应细胞,进一步促进肿瘤细胞的免疫逃逸。结论子宫内膜癌患者CD4+CD25+Treg细胞明显上调,且在肿瘤组织局部表现更为明显,这可能参与了肿瘤的免疫逃逸,促进肿瘤生长和演进,机制可能与IL-10、TGF-β及CCR4表达上调有关。
Objective To investigate the relationship between the level of CD4 + CD25 + Treg cells and the occurrence and development of endometrial carcinoma in peripheral blood and cancer tissues of patients with endometrial carcinoma and its mechanism of action in tumor immune escape. Methods Peripheral blood of 26 patients with endometrial carcinoma was isolated by Ficoll gradient centrifugation and freshly resected surgically resected tumor tissues were used for the preparation of tumor - infiltrating lymphocytes and non - tumor infiltrating lymphocytes. The distribution of CD4 + CD25 + Treg cells was analyzed by flow cytometry. The proportion of CD4 + CD25 + Treg cells in peripheral blood of 25 age-matched healthy controls was used as a control. Treg cells Secreted inhibitory cytokines IL-10 and transforming growth factor (TGF-β) levels and chemokine receptor CCR4 levels. Results The proportion of CD4 + CD25 + Treg cells in patients with endometrial carcinoma was significantly higher than that in adjacent non-cancerous tissues and the control group (P <0.05). The levels of IL-10 and TGF-β in patients with endometrial carcinoma were significantly higher than those in the control group, TGF-β and other inhibitory cytokines and cell-contact inhibition pathway, inhibit immune effector cells, to further promote the immune escape of tumor cells. Conclusion CD4 + CD25 + Treg cells in endometrial carcinoma patients were significantly upregulated, and the expression of CD4 + CD25 + Treg cells was more obvious in tumor tissues, which may be involved in the immune escape of tumor and promote tumor growth and progression. The mechanism may be related to IL-10, TGF- And CCR4 upregulation related.