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目的观察tm TNF-α/TNFR2信号轴对荷瘤鼠肿瘤生长影响及其机制。方法采用Western blot检查H22荷瘤鼠肿瘤微环境中Treg细胞TNFR1及TNFR2的表达。TNFR2敲除BALB/c小鼠和野生型鼠各10只,在TNFR2敲除的BALB/c小鼠皮下接种H22肝癌细胞株,观察肿瘤直径及肿瘤微环境中Treg的募集数量,同时以野生型小鼠做对照。用tm TNF-α刺激Treg细胞,ELISA检测上清IL-10和TGF-β的含量。结果荷瘤鼠微环境中Treg细胞TNFR2表达明显高于野生型小鼠脾脏Treg细胞(P<0.05),而TNFR1表达未见明显变化;TNFR2基因敲除鼠肿瘤直径明显低于野生型小鼠(P<0.05),且肿瘤微环境中Treg细胞数量也明显少于野生型小鼠(P<0.05)。在体外tm TNF-α可以促进Treg细胞产生IL-10和TGF-β(P<0.05)。结论 TNFR2基因敲除小鼠肿瘤生长减缓,肿瘤局部微环境中Treg细胞减少,同时tm TNF-α能够刺激Treg细胞释放抑炎因子IL-10和TGF-β,增强其免疫抑制功能。
Objective To observe the effect of tm TNF-α / TNFR2 signal axis on the tumor growth of tumor-bearing mice and its mechanism. Methods The expression of TNFR1 and TNFR2 in Treg cells in tumor microenvironment of H22-bearing mice was detected by Western blot. TNFR2 knockout BALB / c mice and wild-type mice each 10, in BALB / c mice knockout BALB / c mice were inoculated subcutaneously H22 hepatocellular carcinoma cell lines to observe tumor diameter and tumor microenvironment Treg recruitment, while wild type Mice as a control. Treg cells were stimulated with TNF-α, and the contents of IL-10 and TGF-β in supernatant were detected by ELISA. Results The expression of TNFR2 in Treg cells in tumor-bearing mice was significantly higher than that in wild-type mice (P <0.05), while the expression of TNFR1 did not change significantly. The tumor diameter of TNFR2 knock-out mice was significantly lower than that of wild-type mice P <0.05), and the number of Treg cells in tumor microenvironment was significantly less than that in wild-type mice (P <0.05). Tumor necrosis factor-α (TNF-α) promoted the production of IL-10 and TGF-β in Treg cells in vitro (P <0.05). Conclusions Tumor necrosis factor (TNF) -2 knockout (TNFR2) knockout mice can slow down the growth of Treg cells in the local microenvironment while tm TNF-α can stimulate Treg cells to release anti-inflammatory cytokines IL-10 and TGF-β.