TR60和TR80肿瘤坏死因子受体可独立介导细胞溶解。

Lymphokine and cytokine research Pub Date : 1993-06-01
M Grell, P Scheurich, A Meager, K Pfizenmaier
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引用次数: 0

摘要

人横纹肌肉瘤细胞系KYM-1共表达大量肿瘤坏死因子α (TNF)受体TR60和TR80,对TNF诱导的细胞毒性高度敏感。我们在这里表明,每种受体类型都可以在选择性刺激下自行介导细胞毒性。这是使用受体特异性抗体实现的,能够与相应受体分子的配体结合竞争。因此,tr60特异性单克隆抗体H398在次级交联免疫球蛋白存在下具有强烈的激动性,即细胞毒性。通过抗体介导的受体交联选择性刺激TR80也可诱导KYM-1细胞产生强烈的细胞毒性。有趣的是,当两个受体亚群通过有限的受体交联平行刺激时,观察到加性细胞溶解效应。在每种情况下,各自的Fab片段没有表现出激动活性。当使用天然配体TNF诱导细胞溶解时,受体特异性Fab片段的阻断研究表明,TNF的主要细胞毒性作用是通过TR60介导的,尽管这些受体仅占TNF受体总数的8%左右。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TR60 and TR80 tumor necrosis factor (TNF)-receptors can independently mediate cytolysis.

The human rhabdomyosarcoma cell line KYM-1 coexpresses high numbers of both tumor necrosis factor-alpha (TNF) receptors, TR60 and TR80, and is highly sensitive to TNF-induced cytotoxicity. We show here that each receptor type can mediate cytotoxicity on its own on selective stimulation. This was achieved using receptor specific antibodies, able to compete with ligand binding to the respective receptor molecules. Thus, the TR60-specific monoclonal antibody H398 was strongly agonistic, i.e., cytotoxic, in the presence of a secondary cross-linking immunoglobulin. Selective stimulation of TR80 by antibody-mediated receptor crosslinking also induced strong cytotoxicity in KYM-1 cells. Interestingly, when both receptor subsets were stimulated in parallel by limited receptor cross-linking, additive cytolytic effects were observed. In each case the respective Fab fragments showed no agonistic activity. When the natural ligand TNF was used to induce cytolysis, blocking studies with receptor specific Fab fragments indicated that the main cytotoxic effect of TNF is mediated via TR60, although these receptors represent only about 8% of the total TNF receptor number.

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