Tachibana T, Dei T
Tokai J Exp Clin Med. 1983 Dec;8(5-6):455-63.
Some somatic hybrid cells prepared by cell fusion of MC-induced primary tumor cells with 8-azaguanine resistant L cells were immunogenic in the induction of specific resistance in syngeneic normal mice to the challenge of parental tumor cells. However, inoculations of immunogenic hybrid cells in tumor-bearing hosts evoked enhancement of tumor growth. In these mice with enhanced tumors, the level of immune complexes and antitumor antibodies in sera was more markedly elevated than in sera of untreated tumor-bearers, despite generation of effective cytotoxic T cells in the spleen. Enhancement was not observed by pretreatment with cyclophosphamide (CY), followed by treatment with hybrid cells, but tumor regression occurred. Complete tumor regression was observed in about 70% of animals treated with CY (100 mg/kg) plus viable hybrid cells (10(6)) three times at weekly intervals starting 1 week after tumor transplantation. Coincidental decreases of immune complexes and antitumor antibodies in sera were observed. The results suggest that suppression of the immunological escape mechanism is of primary importance in active tumor-specific immunotherapy.
通过将甲基胆蒽诱导的原发性肿瘤细胞与对8-氮杂鸟嘌呤具有抗性的L细胞进行细胞融合制备的一些体细胞杂种细胞，在同基因正常小鼠中诱导对亲本肿瘤细胞攻击的特异性抗性方面具有免疫原性。然而，在荷瘤宿主中接种免疫原性杂种细胞会引起肿瘤生长的增强。在这些肿瘤增强的小鼠中，尽管脾脏中产生了有效的细胞毒性T细胞，但血清中免疫复合物和抗肿瘤抗体的水平比未治疗的荷瘤小鼠血清中更明显地升高。用环磷酰胺（CY）预处理后再用杂种细胞治疗未观察到增强作用，但出现了肿瘤消退。在肿瘤移植后1周开始，每周3次用CY（100mg/kg）加活的杂种细胞（10⁶）治疗的动物中，约70%观察到完全肿瘤消退。同时观察到血清中免疫复合物和抗肿瘤抗体的减少。结果表明，抑制免疫逃逸机制在主动肿瘤特异性免疫治疗中至关重要。
