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目的研究抗ＣＤ３单克隆抗体与ＩＬ－２共同诱导的Ｔ－ＡＫ细胞和ＩＬ－２脂质体（Ｌ－ＩＬ－２）联合硒酸酯多糖（ＫＳＣ）对Ｌ１２１０小鼠白血病的治疗作用。方法用ＤＢＡ／２小鼠建立Ｌ１２１０白血病模型，正常小鼠脾细胞诱生制备Ｔ－ＡＫ细胞，按设计方案转输Ｔ－ＡＫ细胞和ＩＬ－２脂质体，ＫＳＣ灌胃，检测ＮＫ细胞活性、脾淋巴细胞增殖活性和ＩＬ－２诱生水平，观察荷瘤小鼠生存期。结果Ｌ１２１０白血病小鼠的免疫功能急剧降低，生存期为１６．４３±１．９２天；转输Ｔ－ＡＫ细胞（５×１０６）和Ｌ－ＩＬ－２（１０４Ｕ／ｋｇ）能部分逆转白血病小鼠低下的细胞免疫功能，生存期延长（２４．７８±３．９４天），并有１４．３％小鼠长期存活；ＫＳＣ（４０ｍｇ／ｋｇ）对Ｔ－ＡＫ／Ｌ－ＩＬ－２的抗白血病作用有明显的增强效应，荷瘤小鼠细胞免疫功能进一步增强，生命延长率、长期存活率分别提高３６％和９９．９％。结论硒酸酯多糖具有生物反应调节剂（ＢＲＭ）样作用；以应用Ｔ－ＡＫ细胞和ＩＬ－２脂质体为主体，硒酸酯多糖为辅佐的生物治疗方案对白血病小鼠具有显著的免疫抑瘤作用
Objective To investigate the therapeutic effect of T-AK cells and IL-2 liposome (L-IL-2) combined with selenate ester polysaccharide (KSC) induced by anti-CD3 monoclonal antibody and IL-2 on L1210 mouse leukemia. Methods The model of L1210 leukemia was established by using DBA / 2 mice. T-AK cells were induced from splenocytes of normal mice. T-AK cells and IL-2 liposomes were transplanted as designed. , Splenic lymphocyte proliferative activity and IL-2 induced level, to observe the survival of tumor-bearing mice. Results The immune function of L1210 leukemia mice was drastically reduced and the survival time was 16.43 ± 1.92 days. The transfection of T-AK cells (5 × 106) and L-IL-2 (104U / kg) The survival time was prolonged (24.78 ± 3.94 days), and 14.3% mice were long-term survived. KSC (40 mg / kg) had no effect on T-AK / L-IL-2 The effect of leukemia was obviously enhanced. The cellular immune function of tumor-bearing mice was further enhanced. The life extension rate and long-term survival rate increased by 36% and 99.9% respectively. Conclusions Selenate polysaccharide has biological response modifier (BRM) -like effect. The biologic treatment program using T-AK cells and IL-2 liposomes as the main body and selenate polysaccharide as adjuvant has significant immunity to leukemia mice Anti-tumor effect