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目的观察CD40信号活化后胃癌细胞株增殖凋亡及其表面分子的变化情况并探讨其生物学意义。方法以高表达CD40分子的胃癌细胞株AGS和低表达CD40分子的BGC-823为研究对象,以可溶性CD40配体(sCD40L)激发细胞CD40信号,流式细胞术测定激发CD40信号前后胃癌细胞表面PD-L1分子的表达情况和CD8+T淋巴细胞的表型变化;采用台盼蓝染色法比较CD40活化前后胃癌细胞对CD8+T淋巴细胞的抑制效应。结果 1)CD40信号活化可以诱导高表达CD40分子的胃癌细胞株AGS周期阻滞;2)CD40信号活化可上调AGS细胞表面PD-L1分子的表达,而对低表达CD40分子的细胞BGC-823无上调效应。3)AGS细胞表面PD-L1分子上调明显抑制CD8+T淋巴细胞的增殖并下调其表面CD25分子的表达。结论 CD40信号活化可上调胃癌细胞表面PD-L1表达,继而诱导效应细胞的数量和功能下降,最终有利于胃癌发生免疫逃逸。
OBJECTIVE: To observe the proliferation and apoptosis of gastric cancer cell lines activated by CD40 signaling and the changes of their surface molecules, and to explore their biological significance. Methods The gastric cancer cell line AGS highly expressing CD40 and BGC-823 low expressing CD40 molecule were used as the research objects. CD40 signal was stimulated by soluble CD40 ligand (sCD40L). The surface PD of gastric cancer cells before and after CD40 signal was stimulated by flow cytometry -L1 and the phenotype of CD8 + T lymphocytes. The inhibitory effect of gastric cancer cells on CD8 + T lymphocytes before and after CD40 activation was compared by trypan blue staining. Results 1) The activation of CD40 signal induced AGS cycle arrest in gastric cancer cell lines with high expression of CD40 molecules; 2) Activation of CD40 signaling could up-regulate the expression of PD-L1 on AGS cells, but inhibited the expression of CD40 on BGC-823 cells Up effect. 3) Upregulation of PD-L1 on AGS cells significantly inhibited the proliferation of CD8 + T lymphocytes and down-regulated the expression of CD25 on the surface of AGS cells. Conclusion Activation of CD40 may up-regulate the expression of PD-L1 on the surface of gastric cancer cells, and then induce the decrease of the number and function of effector cells, which ultimately contributes to immune escape in gastric cancer.