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大鼠乳腺腺癌13762的一种对6-硫鸟嘌呤耐药的变体,其免疫原性更强。

A 6-thioguanine-resistant variant of the rat mammary adenocarcinoma 13762 that is more immunogenic.

作者信息

Hoon D S, Ramshaw I A

出版信息

Cancer Immunol Immunother. 1987;24(1):42-8. doi: 10.1007/BF00199831.

Abstract

A 6-thioguanine-resistant (TgR) variant of the metastatic mammary tumor 13762 was found to be very immunogenic. This TgR variant was nontumorigenic and nonmetastatic, whereas the parent 13762 cell line is very tumorigenic and metastatic in normal syngeneic animals. The TgR variant was tumorigenic in irradiated animals. The mechanism of the hosts' immune rejection of this TgR variant was investigated. A 51Cr-release cytotoxic cell assay was used to assess lymphocyte cell-mediated cytotoxicity (CMC) of tumor-draining lymph nodes and spleens from animals injected with tumor cells. In a secondary CMC response of splenic T cells from animals injected with TgR cells, there was a much stronger response as compared to animals injected with 13762 cells. This strong cytotoxic T cell response was short-term and correlated to the host rejection of TgR cells. Previously, we selected revertant cell lines (TgRrev, TgRrevM) from the TgR variant line that were more metastatic and tumorigenic. The revertant cell lines induced a lower CMC response than the TgR line, but a higher response compared to the parent 13762 line. The poor CMC response from 13762 tumor-bearing animals was investigated and appeared to be due to a suppressor T cell response.

摘要

转移性乳腺肿瘤13762的一种6-硫鸟嘌呤抗性(TgR)变体被发现具有很强的免疫原性。这种TgR变体不具有致瘤性和转移性,而亲本13762细胞系在同基因正常动物中具有很强的致瘤性和转移性。TgR变体在受辐照动物中具有致瘤性。对宿主免疫排斥该TgR变体的机制进行了研究。采用51Cr释放细胞毒性试验来评估注射肿瘤细胞的动物肿瘤引流淋巴结和脾脏的淋巴细胞介导的细胞毒性(CMC)。在注射TgR细胞的动物脾脏T细胞的二次CMC反应中,与注射13762细胞的动物相比,反应要强得多。这种强烈的细胞毒性T细胞反应是短期的,并且与宿主对TgR细胞的排斥相关。此前,我们从TgR变体系中筛选出了转移性和致瘤性更强的回复细胞系(TgRrev、TgRrevM)。回复细胞系诱导的CMC反应比TgR系低,但比亲本13762系高。对13762荷瘤动物的CMC反应较差的情况进行了研究,发现这似乎是由于抑制性T细胞反应所致。

相似文献

本文引用的文献

1
Heritable alterations in tumor-cell immunogenicity.肿瘤细胞免疫原性的可遗传改变。
Immunol Today. 1982 Feb;3(2):34-6. doi: 10.1016/0167-5699(82)90057-3.

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