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目的：为探讨ＤＢＡ／２小鼠脾淋巴细胞诱生的抗ＣＤ３单克隆抗体（单抗）激活的杀伤细胞（ＣＤ３ＡＫ细胞）过继输入及联合化疗和生物反应调节剂对小鼠白血病的治疗作用。方法：将Ｐ３８８细胞移植到ＤＢＡ／２小鼠腹腔建立白血病模型，用抗ＣＤ３单抗和小剂量重组白细胞介素２（ｒＩＬ－２）从小鼠脾细胞中诱生ＣＤ３ＡＫ细胞。检测淋巴细胞转化率、ＮＫ细胞活性和脾淋巴细胞ＩＬ－２诱生水平以及荷瘤鼠生存期。结果：小鼠接种Ｐ３８８细胞后细胞免疫功能（淋巴细胞转化率、ＮＫ活性和ＩＬ－２水平）明显减低。转输ＣＤ３ＡＫ细胞和小剂量ｒＩＬ－２，小鼠生存期延长（４５．１９％），细胞免疫功能显著增强；单纯化疗可以延长小鼠生存期（２９．９０％），但却使免疫功能低下的荷瘤鼠的Ｔ细胞和ＮＫ细胞功能进一步降低，与ＣＤ３ＡＫ细胞转输联合可阻止化疗所致的免疫功能的降低，生存期进一步延长（５９．４５％），并有２５％的小鼠长期存活；硒酸酯多糖与ＣＤ３ＡＫ细胞或ＣＤ３ＡＫ细胞＋化疗联合应用治疗效果最佳，１２．５％～７５．０％小鼠长期存活，且体内未发现有白血病细胞存在。结论：硒酸酯多糖是一种实用而有效的生物反应调节剂，肿瘤杀伤效应细胞＋化疗＋生物反应调节剂方案是一种白?
OBJECTIVE: To investigate the therapeutic effect of adoptive infusion of anti-CD3 monoclonal antibody (mAb) -activated killer cells (CD3AK cells) induced by splenic lymphocytes of DBA / 2 mice and the combined chemotherapy and biologic response modifier on mouse leukemia. Methods: P388 cells were transplanted into the peritoneal cavity of DBA / 2 mice to establish leukemia model. CD3AK cells were induced from mouse spleen cells with anti-CD3 monoclonal antibody and low dose recombinant interleukin-2 (rIL-2). Lymphocyte transformation rate, NK cell activity and splenic lymphocyte IL-2 induced levels and tumor-bearing mice survival were detected. Results: The cellular immune function (lymphocyte transformation rate, NK activity and IL-2 level) in P388 cells was significantly decreased. CD3AK cells and low-dose rIL-2 could prolong the survival of mice (45.19%) and significantly improve the cellular immune function. The chemotherapy alone could prolong the survival of mice (29.90%), but the immunocompromise Of tumor-bearing mice further reduced the function of T cells and NK cells, and the combination with CD3AK cells prevented the decrease of immune function induced by chemotherapy and prolonged the survival time (59.45%), and 25% Survival; selenate polysaccharide and CD3AK cells or CD3AK cells + chemotherapy combined with the best treatment effect, 12.5% ~ 75.0% mice long-term survival, and no leukemia cells found in vivo. Conclusion: Selenite polysaccharide is a practical and effective biological response modifier. The program of tumor killing effector cell + chemotherapy + biological response modifier is a kind of white?