肿瘤坏死因子对急性白血病LAK细胞抗肿瘤活性的增强作用

ENHANCING EFFECT OF TUMOR NECROSIS FACTOR(TNF)ON THE ANTLEUKEMIA ACTIVITY OF LAK CELLS

采用基因重组肿瘤坏死因子（ＴＮＦ）与白细胞介素２（ＩＬ－２）联合诱导急性白血病患者外周血单个核细胞，结果表明：ＴＮＦ（５００Ｕ／ｍｌ）单独不能诱导出ＬＡＫ细胞活性，也不能进一步提高最适剂量ＩＬ－２（１０００Ｕ／ｍｌ）诱导的ＬＡＫ细胞活性，但能显著增强亚适剂量ＩＬ－２（１０～１００Ｕ／ｍｌ）诱导的ＬＡＫ细胞活性。抗ＴＮＦ单抗和抗ＩＬ－２受体β链（Ｐ＿（７５））单抗能显著抑制ＴＮＦ／ＩＬ－２对ＬＡＫ细胞活性的协同诱导作用。ＴＮＦ与ＬＡＫ细胞联合可显著增强对白血病细胞的杀伤活性。

eripheral blood mononuclear cells(PMBNC)of pa-dents with acute leukemia were induced by interleukin-2(IL-2)and TNF.It was found that TNF(500U/ml)alone was unable to induce LAK activity and could not enhance the LAK activity induced by IL-2 at optimalconcentration(1000U/ml),but it could increase the LAK activity induced by suboptimaldose IL-2(10～100U/ml).The TNF/IL-2‘synergistic effect on LAKactivity was significantly inhibited by anti-TNF McAb(Z_8)or anti-IL-2Rβchain McAb (TU_(27).In addition,the antileukemia activities ofTNFand LAK cell could be markedly augmented when they acted together.