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目的研究乳腺癌细胞系MCF-7和MDA-MB-231细胞NK细胞活化性配体表达和细胞因子诱导的杀伤细胞(CIK)杀伤敏感性。方法采用流式细胞术检测MCF-7和MDA-MB-231细胞表面MICA、MICB、CD155和CD112的表达,PBMC在体外经γ-干扰素(IFN-γ),CD3抗体和IL-2诱导扩增为CIK细胞,乳酸脱氢酶释放法检测CIK细胞对MCF-7和MDA-MB-231细胞的杀伤活性。结果 MICA、MICB、CD155和CD112在MCF-7细胞表面的表达水平均明显高于MDA-MB-231细胞(P<0.01);培养15 d后,CIK细胞中CD3+CD56+细胞百分率显著增高(P<0.01);效靶比20:1时,CIK细胞对MDA-MB-231细胞的杀伤率高于其对MCF-7细胞的杀伤率,差异显著(P<0.01)。结论 CIK细胞对MCF-7和MDA-MB-231的杀伤活性不依赖于NK细胞活化性配体分子MICA、MICB、CD155和CD112的高表达;CIK过继免疫细胞治疗可能成为三阴乳腺癌的有效治疗手段。
Objective To investigate the expression of NK cell-activating ligand and cytokine-induced killer (CIK) cytotoxicity in human breast cancer cell lines MCF-7 and MDA-MB-231. Methods The expressions of MICA, MICB, CD155 and CD112 on MCF-7 and MDA-MB-231 cells were detected by flow cytometry. PBMCs were induced by IFN-γ, CD3 and IL- Increased CIK cells, lactate dehydrogenase release assay CIK cells on MCF-7 and MDA-MB-231 cell killing activity. Results The expression levels of MICA, MICB, CD155 and CD112 on MCF-7 cells were significantly higher than those on MDA-MB-231 cells (P <0.01), and the percentage of CD3 + CD56 + cells in CIK cells was significantly increased <0.01). When the target ratio was 20: 1, the cytotoxicity of CIK cells to MDA-MB-231 cells was higher than that of CIK cells to MCF-7 cells (P <0.01). Conclusion The cytotoxicity of CIK cells to MCF-7 and MDA-MB-231 is independent of the high expressions of MICA, MICB, CD155 and CD112, and the adoptive immunotherapy of CIK cells may be effective in treating triple-negative breast cancer treatment approach.