诱导肿瘤细胞产生单因子。

Lymphokine research Pub Date : 1989-01-01
D N Männel, R Jänicke
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引用次数: 0

摘要

红细胞原系K562和T细胞系Jurkat能够诱导体外人外周血源性单核细胞中TNF-、IL1 α -和IL1 β - mrna表达的增加。这些肿瘤细胞的激活原理与不同分子质量的膜制剂组分有关,Jurkat细胞为32-38 kD, K562细胞为46-54 kD。至少部分的激活成分似乎是蛋白质。两种细胞类型的分离膜制剂均可诱导TNF的产生和分泌。只有当使用Jurkat细胞时,活的肿瘤细胞刺激单核细胞导致TNF释放。活的K562细胞诱导TNFmRNA表达增强,但似乎从上清中吸收可溶性TNF。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Induction of monokine production by tumor cells.

Cells of the proerythromyeloid cell line K562 and of the T cell line Jurkat were able to induce an increase in TNF-, IL1 alpha-, and IL1 beta-mRNA expression in human peripheral blood derived monocytes in vitro. The activating principle of these tumor cells was associated with fractions of membrane preparations of distinct molecular mass, 32-38 kD for Jurkat cells and 46-54 kD for K562 cells, respectively. At least part of the activating constituent seemed to be protein in nature. Isolated membrane preparations of both cell types induced production and secretion of TNF. Stimulation of monocytes with the viable tumor cells led to TNF release only when Jurkat cells were used. Viable K562 cells induced enhanced TNFmRNA expression but seemed to absorb soluble TNF from the supernatant.

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