Abstract in English, Chinese Objective: To study if programmed death-ligand 1 (PL-L1) expression in breast cancer cell activates PD-L1/PD-1 pathway in dendritic cells to inhibit dendritic cell maturation. Methods: Human monocytes were induced to differentiate into immature dendritic cells using GM-CSF and IL-4, and further to mature dendritic cells using TNF-α. PD-L1-expressing breast cancer cell line MDA-MB-231 was co-cultured in contact with the dendritic cells to observe the effects of the breast cancer cells on the maturation of the dendritic cells. A PD-L1 blocking antibody was applied to the co-culture, and the changes in the inhibitory effect of the MDA-MB-231 cells on dendritic cell maturation was observed. TNF-α-induced dendritic cells were treated with a recombinant human PD-L1 protein to study the effect of PD-L1/PD-1 pathway activation on the maturation of dendritic cells. The expression of PD-L1 in MDA-MB-231 cells and the dendritic cell maturation marker HLA-DR and CD83 were analyzed using flow cytometry. Results: MDA-MB-231 cell line showed PD-L1 positivity on the cell membrane cells at a rate as high as (99.7∓0.15)%. In mature dendritic cells, the positivity rates for HLA-DR and CD83 were (88.8∓6.96)% and (18.36∓3.07)%, respectively, but in the co-culture system, the positivity rates of the dendritic cells were significantly decreased to (42.76∓10.52)% (P<0.01) and (9.93∓2.74)% (P<0.05), respectively, indicating that MDA-MB-231 cells inhibited the maturation of dendritic cells. Following treatment with a PD-L1 antibody isotype control, the percentages of HLA-DR- and CD83-positive cells in the co-culture were (45.17∓10.19)% and (10.15∓2.54)%, which were significantly increased to (63.46∓1.72)% and (16.46∓2.58)% after treatment with PD-L1 antibody, respectively (both P<0.05). Compared with the mature dendritic cell controls, the cells treated with the recombinant human PD-L1 protein exhibited significantly lowered percentages of HLA-DR-positive [from (84.23∓4.18)% to (2.56∓2.39)%, P<0.05] and CD83-positive cells [(87.26∓1.54)% to (60.67∓1.63)%, P<0.05]. Conclusion: The effect of PD-L1 antibody therapy on triple negative breast cancer can be partially mediated by blocking PD-L1 expression on breast cancer cell membrane, which attenuates the inhibition of dendritic cell maturation in the cancer microenvironment. 目的: 探讨表达PD-L1的乳腺癌细胞是否通过激活树突状细胞的PD-L1/PD-1信号通路抑制树突状细胞成熟。 方法: 人单核细胞用GM-CSF和IL-4诱导为不成熟树状突细胞, 再用TNF-α诱导为成熟树状突细胞; 表达PD-L1的乳腺癌细胞系MDAMB-231与树状突细胞接触共培养; PD-L1阻断抗体处理共培的的乳腺癌细胞和树状突细胞; 重组人PD-L1蛋白处理TNF-α诱导的树突状细胞; 流式细胞仪检测乳腺癌细胞膜PD-L1的表达和树突状细胞的成熟分化标志HLA-DR和CD83。 结果: 乳腺癌细胞MDA-MB-231细胞系中, 细胞膜表面PD-L1阳性细胞高达(99.7±0.15) %; HLA-DR和CD83阳性细胞在成熟树状突细胞对照组分别为(88.8±6.96) %和(18.36±3.07) %, 在MDA-MB-231共培养实验组树状突细胞群分别降至(42.76±10.52) %和(9.93± 2.74) %, 两组比较差异有统计学意义(P < 0.01, P < 0.05); HLA-DR和CD83阳性细胞在PD-L1抗体同型对照组分别为(45.17± 10.19) %和(10.15±2.54) %, 在PD-L1抗体处理组分别升至(63.46±1.72) %和(16.46±2.58) %, 两组相比差异均有统计学意义(P < 0.05);和成熟树状突细胞对照组相比, 人重组PD-L1蛋白处理组HLA-DR和CD83阳性细胞率较低, 组间统计学差异有统计学意义(P < 0.05)。 结论: PD-L1抗体对三阴性乳腺癌患者的治疗的效果, 可能部分基于抗体阻断乳腺癌细胞表面的PD-L1, 从而减弱其对肿瘤微环境中的树突状细胞成熟的抑制作用。