CAJ | 학술논문

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。
목적：연구유선암세포계MCF-7화MDA-MB-231세포NK세포활화성배체표체화세포인자유도적살상세포( CIK)살상민감성。방법채용류식세포술검측 MCF-7화 MDA-MB-231세포표면 MICA、MICB、CD155화CD112적표체,PBMC재체외경γ-간우소( IFN-γ), CD3항체화IL-2유도확증위CIK세포,유산탈경매석방법검측CIK세포대MCF-7화MDA-MB-231세포적살상활성。결과 MICA、MICB、CD155화CD112재MCF-7세포표면적표체수평균명현고우MDA-MB-231세포( P<0．01)；배양15 d후, CIK세포중CD3+CD56+세포백분솔현저증고( P<0．01)；효파비20：1시,CIK세포대MDA-MB-231세포적살상솔고우기대MCF-7세포적살상솔,차이현저(P<0．01)。결론 CIK세포대 MCF-7화 MDA-MB-231적살상활성불의뢰우 NK 세포활화성배체분자 MICA、MICB、CD155화CD112적고표체；CIK과계면역세포치료가능성위삼음유선암적유효치료수단。
Objective To study the ligand expressions of NK cell ( nature killer cell) activation in MCF-7 and MDA-MB-231 cells in breast carcinoma cell line and sensitivity of CIK ( cytokine-induced killer) cells. Methods The expressions of MICA, MICB, CD155 and CD112 on MCF-7 and MDA-MB-231 cells were detected by flow cytometry. CIK cells were obtained by the sequential ex vivo expansion of peripheral blood mononuclear cells ( PBMC) with interfer-on-gamma (IFN-γ), and anti-CD3 antibody and recombinant human interleukin (IL)-2. The cytotoxicity of CIK cells a-gainst MCF-7 and MDA-MB-231 cells were detected by lactate dehydrogenase ( LDH) release assay. Results The ex-pressions of MICA, MICB, CD155 and CD112 on MCF-7 cells were significantly higher than those on MDA-MB-231 cells (P<0. 01);after 15 d of ex vivo expansion, the percentage of CD3+CD56+ cell increased significantly (P<0. 01);at E:T ratios of 20:1, the cytotoxicity of CIK cells against MDA-MB-231 was significantly higher than that against MCF-7 (P<0. 01). Conclusion The cytotoxicity of CIK cells against MCF-7 and MDA-MB-231 cells is independent of over-expressions of MICA, MICB, CD155 and CD112. CIK adoptive immunity of cell therapy may be an effective approach for treatment of triple-negative breast cancer.