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目的探讨白细胞介素7(IL7)对急性白血病(AL)细胞B7分子表达和免疫原性的影响。方法用流式细胞术检测AL原代白血病细胞B7分子的表达。体外用IL7诱导白血病细胞,分析其对B7分子蛋白表达的影响,进而用RTPCR检测B71和B7-2mRNA表达。MTT法检测诱导后白血病细胞对异基因外周血单个核细胞(PBMNC)的刺激作用,并用酶联免疫吸附法(ELISA)测定上清液中γ干扰素(IFNγ)含量。应用B71、B72和W6/32单抗阻断实验研究B7分子刺激PBMNC的机制。结果11例AL患者中B71弱阳性3例,B7-2弱阳性1例。IL7能显著刺激白血病细胞B7-1和B72表达,呈时间依赖性。IL7作用于HL60细胞可诱导B71和B72mRNA表达。诱导后的白血病细胞显著刺激PBMNC增殖并产生IFNγ。B71单抗和W6/32单抗可抑制白血病细胞诱导PBMNC增殖和产生IFNγ,而B7-2单抗无抑制作用。结论原代AL细胞低表达B71和B72分子。在体外,IL7通过诱导白血病细胞B71分子表达,刺激淋巴细胞增殖,使PBMNC分泌IFNγ增多,显著提高了白血病细胞的免疫原性。在共刺激分子诱导抗白血病T细胞免疫反应中,B71作用显著强于B7-2。
Objective To investigate the effect of interleukin 7 (IL7) on B7 expression and immunogenicity in acute leukemia (AL) cells. Methods Flow cytometry was used to detect the expression of B7 in AL primary leukemia cells. In vitro, leukemia cells were induced with IL7, and their effects on the expression of B7 protein were analyzed. The expression of B71 and B7-2 mRNA was detected by RTPCR. Stimulation of leukemic cells on allogeneic peripheral blood mononuclear cells (PBMNC) after induction was detected by MTT assay. The content of IFN-γ in supernatant was determined by enzyme-linked immunosorbent assay (ELISA). B71, B72 and W6 / 32 mAb blocking experiments using B7 molecules stimulate PBMNC mechanism. Results In 11 AL patients, B71 was weakly positive in 3 cases and B7-2 was weakly positive in 1 case. IL7 can significantly stimulate leukemia cells B7-1 and B72 expression in a time-dependent manner. IL7 can induce B71 and B72 mRNA expression in HL60 cells. The induced leukemic cells significantly stimulated PBMNC proliferation and IFNγ production. B71 mAb and W6 / 32 mAb inhibited leukemia cells from inducing PBMNC proliferation and IFNγ production, whereas B7-2 mAb had no inhibitory effect. Conclusion Primary AL cells express low levels of B71 and B72 molecules. In vitro, IL7 stimulates the proliferation of lymphocytes by inducing the expression of B71 in leukemia cells, increases the secretion of IFNγ by PBMNC, and significantly enhances the immunogenicity of leukemic cells. In costimulatory molecules induced anti-leukemia T cell immune response, B71 was significantly stronger than B7-2.