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用环磷酰胺耗尽小鼠体内的抑制性T细胞对SV40诱导的肿瘤相关抗原的特异性细胞介导细胞毒性反应的调节

Regulation of specific cell-mediated cytotoxic response against SV40-induced tumor associated antigens by depletion of suppressor T cells with cyclophosphamide in mice.

作者信息

Glaser M

出版信息

J Exp Med. 1979 Mar 1;149(3):774-9. doi: 10.1084/jem.149.3.774.

Abstract

When cyclophosphamide was administered to mice before immunization with syngeneic SV40 transformed cells, the specific immune response elicited, as was measured by in vitro 51Cr release assay was stronger and lasted longer when compared to the response generated in noncyclophosphamide-treated mice. The augmentation effect of the drug was dependent on cyclophosphamide concentration being optimal at 100 mg/kg and on the time of drug administration in relation to antigen immunization being optimal at 2 d before antigen administration. Transfer of T cells from normal syngeneic mice to drug-treated animals abolished the cyclophosphamide-induced augmentation of immune response. These results implied that cyclophosphamide sensitive T cells suppressed the in vivo generation of specific effector T cells against SV40-induced tumor-associated antigens.

摘要

在用同基因SV40转化细胞免疫小鼠之前给其注射环磷酰胺,通过体外51Cr释放试验测定发现,与未用环磷酰胺处理的小鼠所产生的反应相比,所引发的特异性免疫反应更强且持续时间更长。该药物的增强作用取决于环磷酰胺浓度在100mg/kg时最佳,且取决于相对于抗原免疫的给药时间,在抗原给药前2天最佳。将正常同基因小鼠的T细胞转移到经药物处理的动物体内,消除了环磷酰胺诱导的免疫反应增强。这些结果表明,对环磷酰胺敏感的T细胞抑制了体内针对SV40诱导的肿瘤相关抗原的特异性效应T细胞的产生。

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