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目的:研究CD4+T细胞克隆特异性杀伤自体非霍奇金淋巴瘤的相关机制。方法:以患者自体恶性淋巴瘤细胞株(M-CH1细胞)为刺激源,培养得到具有特异杀伤性的CD4+T细胞,采用细胞毒试验、细胞毒抗体封闭试验及细胞流式等技术,研究该CD4+T细胞特异杀伤肿瘤的机制。结果:得到的3个特异的CD4+T细胞克隆(5.1、10.4和40.1)均可通过人类白细胞抗原(HLA)-Ⅱ分子中HLA-DP依赖途径杀伤M-CH1细胞。经流式细胞仪分析,证实这些CD4+T细胞克隆并非自然杀伤T细胞(NKT细胞)来源。concanamycin A(CMA)和乙二醇双(2-氨乙基醚)四乙酸(EGTA)能够阻断这些T细胞克隆的特异性肿瘤杀伤作用。同时,这些CD4+T细胞克隆能高表达穿孔素和颗粒酶。结论:在该研究体系中,CD4+T细胞克隆特异性杀伤自体非霍奇金淋巴瘤的机制主要是通过HLA-DP限制性的穿孔素途径。
Objective: To study the mechanism of CD4 + T cell clone-specific killing of non-Hodgkin’s lymphoma. Methods: CD4 + T cells with specific cytotoxicity were obtained by culturing patients with autologous malignant lymphoma cell line (M-CH1 cells). Cytotoxicity test, cytotoxic antibody blocking test and cell flow cytometry were used to study The CD4 + T cell-specific mechanism of killing tumors. Results: All the three specific CD4 + T cell clones (5.1, 10.4 and 40.1) could kill M-CH1 cells through the HLA-DP dependent HLA-Ⅱ pathway. Flow cytometry analysis confirmed that these CD4 + T cell clones were not derived from natural killer T cells (NKT cells). Concanamycin A (CMA) and ethylene glycol bis (2-aminoethyl ether) tetraacetic acid (EGTA) blocked the specific tumor killing of these T cell clones. At the same time, these CD4 + T cell clones are highly capable of expressing perforin and granzyme. CONCLUSIONS: In this study, the mechanism by which CD4 + T cell clones specifically kill autologous non-Hodgkin’s lymphoma is primarily through the HLA-DP-restricted perforin pathway.