Testorelli C, Canti G, Franco P, Goldin A, Nicolin A
Br J Cancer. 1983 Mar;47(3):353-9. doi: 10.1038/bjc.1983.53.
A monoclonal antibody (L.1), reacting in vitro specifically with L1210 leukaemia cells in a complement-dependent cytotoxicity assay (CDC), has been exploited for serotherapy studies. Different regiments of L.1 treatment of CD2F1 mice bearing the semi-syngeneic L1210 leukaemia did not prolong the life span of tumor-bearing animals. Moreover, the administration of L.1 did not enhance the antitumour effects of cyclophosphamide. Studies of in vivo localization showed that L.1 was able to bind specifically to L1210 leukaemic cells, although 30-40% of the cells remained negative. The presence of L.1 in mouse blood was demonstrated up to 15 days after the inoculation. On the other hand, in vivo administration of L.1 was probably accompanied by loss of the cytotoxic activity, perhaps through a mechanism of complement inactivation, since the presence of undiluted normal mouse serum in a CDC assay inhibited the cytotoxic activity of L.1. Moreover, serum from L.1-treated mice did not display any cytotoxic activity, although the presence of the antibody could be demonstrated by indirect immunofluorescence. Shedding of the antigen defined by L.1 was probably not responsible for the failure of the serotherapy, since the L.1 neutralizing antigen could be found in body fluids only long after the start of therapy.
一种单克隆抗体（L.1），在体外补体依赖细胞毒性试验（CDC）中能与L1210白血病细胞特异性反应，已被用于血清疗法研究。对携带半同基因L1210白血病的CD2F1小鼠采用不同方案进行L.1治疗，并未延长荷瘤动物的寿命。此外，给予L.1并未增强环磷酰胺的抗肿瘤作用。体内定位研究表明，L.1能够特异性结合L1210白血病细胞，尽管30 - 40%的细胞仍呈阴性。接种后长达15天在小鼠血液中都能检测到L.1的存在。另一方面，L.1的体内给药可能伴随着细胞毒性活性的丧失，也许是通过补体失活机制，因为在CDC试验中未稀释的正常小鼠血清的存在会抑制L.1的细胞毒性活性。此外，L.1治疗小鼠的血清未显示出任何细胞毒性活性，尽管通过间接免疫荧光可证明抗体的存在。由L.1定义的抗原脱落可能不是血清疗法失败的原因，因为L.1中和抗原在治疗开始很久之后才会在体液中被发现。
