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为检测CD4+CD25brightCCR6+Treg在小鼠乳腺癌实验动物模型中的分布,并探讨其意义。采用FACS检测正常小鼠和4T1荷瘤小鼠中CD4+CD25brightTreg的记忆分子CCR6的表达水平,同时检测CD4+CD25brightTreg的CCR6+和CCR6-两个亚群的Foxp3表达情况;用增殖抑制实验观察了两个亚群分别对CD4+CD25-T细胞增殖的抑制作用;用FACS检测CD4+CD25brightCCR6+Treg在正常小鼠和4T1荷瘤小鼠中PBMC、LN和TIL中的分布情况。结果:4T1荷瘤小鼠中CD4+CD25brightTreg的记忆分子CCR6的表达水平较正常小鼠增加;CD4+CD25brightTreg的CCR6+和CCR6-两个亚群均高表达Foxp3,均能在体外有效抑制CD4+CD25-T细胞的增殖;与正常对照相比,CD4+CD25brightCCR6+Treg在4T1荷瘤模型的引流淋巴结中比例明显增加,并在肿瘤局部存在显著的富集。上述结果提示在肿瘤免疫中存在CD4+CD25brightCCR6+Treg,其具有效应/记忆样表型,并在肿瘤局部有明显的富集,这可能是肿瘤长期免疫逃逸的重要机制。
To detect the distribution of CD4 + CD25brightCCR6 + Treg in mouse mammary cancer experimental animal models and to explore its significance. The expression of CCR6 in CD4 + CD25brightTregs in normal mice and 4T1 tumor-bearing mice was detected by FACS, and Foxp3 expression in both CCR6 + and CCR6- subsets of CD4 + CD25brightTregs was also detected by FACS; Subpopulations of CD4 + CD25-T cells respectively. The distribution of CD4 + CD25brightCCR6 + Tregs in PBMCs, LNs and TILs in normal mice and 4T1 mice was detected by FACS. Results: The expression of CCR6 in CD4 + CD25brightTregs was increased in 4T1 tumor-bearing mice compared with that in normal mice. Both CCR6 + and CCR6- in CD4 + CD25brightTreg overexpressed Foxp3, both in vitro and in vivo, -T cells. Compared with normal controls, CD4 + CD25brightCCR6 + Tregs significantly increased in the draining lymph nodes of 4T1 tumor-bearing model, and there was a significant enrichment in the tumor. The above results suggest that there is CD4 + CD25brightCCR6 + Treg in tumor immunity with effector / memory phenotype and obvious enrichment in the tumor site, which may be an important mechanism of tumor long-term immune escape.