在接受抗独特型抗体的小鼠中，猿猴病毒40转化细胞诱导的体内肿瘤形成受到抑制。
Suppression of in vivo tumor formation induced by simian virus 40-transformed cells in mice receiving antiidiotypic antibodies.
作者信息
Kennedy R C, Dreesman G R, Butel J S, Lanford R E
出版信息
J Exp Med. 1985 Jun 1;161(6):1432-49. doi: 10.1084/jem.161.6.1432.
Abstract
This study characterizes four private idiotypes (Id) associated with monoclonal antibodies (mAb) to simian virus 40 (SV40) tumor antigen (T-Ag), and to a cellular protein, p53. Anti-Id recognized Id determinants associated with the antibody-combining site. BALB/c mice receiving a pool of anti-Id directed against mAb recognizing distinct amino and carboxyl terminal epitopes of T-Ag before receiving a tumorigenic dose of SV40-transformed cells showed suppression of tumor formation. Serum obtained from these mice before tumor challenge contained anti-anti-Id that failed to bind T-Ag. These data support the potential role of regulatory idiotopes in tumor immunity.
摘要
本研究对四种与抗猿猴病毒40（SV40）肿瘤抗原（T-Ag）及一种细胞蛋白p53的单克隆抗体（mAb）相关的独特型（Id）进行了表征。抗独特型识别与抗体结合位点相关的独特型决定簇。在接受致瘤剂量的SV40转化细胞之前，接受针对识别T-Ag不同氨基和羧基末端表位的mAb的抗独特型混合物的BALB/c小鼠显示出肿瘤形成受到抑制。在肿瘤攻击前从这些小鼠获得的血清中含有无法结合T-Ag的抗抗独特型。这些数据支持调节性独特型在肿瘤免疫中的潜在作用。
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本文引用的文献
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