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作 者:吴志懂[1] 覃俊仕[1] 罗汉传[1] 吴瑞正[1] 滕奔宇[1]
机构地区:[1]广西壮族自治区贵港市人民医院肝胆腺体外科,广西贵港537100
出 处:《中国普通外科杂志》2015年第5期701-706,共6页China Journal of General Surgery
基 金:广西省贵港市科学技术局科技攻关资助项目(1408026)
摘 要:目的:探讨乳腺癌患者CD4+CD25+Foxp3+调节性T细胞(简称Foxp3+Treg)的变化及意义。方法:选择40例乳腺癌患者和32例乳腺良性肿瘤患者,采用流式细胞术检测外周血Foxp3+Treg、CD8+CD28+T细胞、NK细胞水平;用Western blot和RT-PCR病变乳腺组织Foxp3蛋白与m RNA表达。结果:乳腺癌患者外周血中Foxp3+Treg比例较乳腺良性肿瘤患者明显升高,而CD8+CD28+T细胞、NK细胞比例明显降低(均P<0.05),且乳腺癌患者外周血Foxp3+Treg水平与CD8+CD28+T细胞和NK细胞水平呈负相关(r=-0.631,r=-0.578,均P<0.05);乳腺癌患者术后外周血Foxp3+Treg水平较术前明显降低(P<0.05)。乳腺癌组织中Foxp3蛋白与m RNA的表达均较乳腺良性肿瘤组织明显升高(均P<0.05)。结论:Foxp3+Treg和其标记分子Foxp3在乳腺癌患者中的表达增加,且可能通过抑制CD8+CD28+T细胞和NK细胞而产生肿瘤免疫抑制。Objective:To investigate the alteration of CD4+CD25+Foxp3+ regulartory T cells(hereinafter abbreviated as Foxp3+ Tregs) in breast cancer patients and its signiifcance.Methods:Forty patients with breast cancer and 32 patients with benign breast tumors were enrolled.The levels of Foxp3+ Tregs,CD8+CD28+ T cells and NK cells in peripheral blood of the patients were measured by l ow cytometry,and the Foxp3 protein and mR NA expressions in breast lesions were determined by Western blot and RT-PCR,respectively.Results:The ratio of Foxp3+ Tregs was signiifcantly higher,while the ratios of both CD8+CD28+ T cells and NK cel s in peripheral blood were significantly lower in breast cancer patients than those in patients with benign breast tumor(all P0.05),and there was a negative correlation between the level of Foxp3+ Tregs and either the level ofCD8+CD28+ T cells or NK cells in peripheral blood of breast cancer patients(r=–0.631,r=–0.578,both P0.05); the peripheral blood level of Foxp3+ Tregs in breast cancer patients was significantly decreased after operation compared with the level before operation(P0.05).Either protein or mR NA level of Foxp3 in breast cancer tissue was signiifcantly higher than that in benign breast tumor tissue(both P0.05).Conclusion:Foxp3+ Treg and its molecular marker Foxp3 are increased in breast cancer patients,which may probably contribute to the tumor immunosuppression through inhibition of CD8+CD28+ T and NK cells.
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