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为探讨乳腺癌患者外周血单个核细胞(PBMC)介导LAK样杀伤作用和ADCC(抗体依赖性细胞介导的细胞毒)作用下降的机制,观察IL-2增强乳腺癌患者PBMC介导杀伤作用的效果。应用MTT法检测LAK样杀伤作用;应用非核素细胞毒试剂盒(LDH释放法)检测ADCC杀伤作用;应用流式细胞术检测CD3+CD8+T细胞、CD3-CD56+NK细胞水平和CD16ζ的表达。结果显示:进展期乳腺癌患者PBMC中CD3+CD8+T细胞、CD3-CD56+NK细胞及其CD16ζ的表达水平与健康对照组相比明显降低,有统计学意义(P<0.01)。进展期乳腺癌患者PBMC经IL-2(1 000 U/ml)处理5 d后,CD3+CD8+T细胞和CD3-CD56+NK细胞比例明显增加,CD16ζ的表达水平明显提高。在各效靶比时,IL-2处理后进展期乳腺癌患者PBMC对SKBR3细胞的LAK样和ADCC杀伤率明显高于未处理组,差异有统计学意义(P<0.01);提示进展期乳腺癌患者PBMC介导的LAK样杀伤活性和ADCC作用明显削弱,CD3+CD8+T细胞、CD3-CD56+NK细胞比例和CD16ζ的表达水平明显降低,IL-2可以刺激CD3+CD8+T细胞和CD3-CD56+NK细胞增殖活化,促进CD16ζ的表达,增强杀伤作用。
To investigate the mechanism of LAK-like cytotoxicity and ADCC (antibody-dependent cell-mediated cytotoxicity) mediated by peripheral blood mononuclear cells (PBMCs) in breast cancer patients and to explore the mechanism of IL-2-induced enhancement of PBMCs in breast cancer patients Effect. The killing effect of LAK was detected by MTT assay. The killing effect of ADCC was detected by non-radionuclide cytotoxic kit (LDH release assay). The levels of CD3 + CD8 + T cells, CD3 + CD56 + NK cells and CD16ζ expression. The results showed that the expression levels of CD3 + CD8 + T cells, CD3-CD56 + NK cells and CD16ζ in PBMC of patients with advanced breast cancer were significantly lower than those in healthy controls (P <0.01). The proportion of CD3 + CD8 + T cells and CD3 + CD56 + NK cells in PBMC of patients with advanced breast cancer was significantly increased after treated with IL-2 (1000 U / ml) for 5 d, and the expression of CD16ζ was significantly increased. At various effect-target ratios, the killing rates of LAK-like cells and ADCC in SKBR3 cells from PBMCs of patients with advanced breast cancer after IL-2 treatment were significantly higher than those of untreated patients (P <0.01), suggesting that breast cancer CD3 + CD8 + T cells, CD3-CD56 + NK cells and CD16ζ expression were significantly decreased in PBMCs of patients with cancer, and IL-2 could stimulate CD3 + CD8 + T cells and CD3-CD56 + NK cell proliferation and activation, promote CD16ζ expression, enhance the killing effect.