肿瘤坏死因子-α可诱导人胶质母细胞瘤U87-MG细胞对自然杀伤细胞介导的裂解作用的敏感性增加。
Tumour necrosis factor-alpha induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis.
作者信息
Kondo S, Yin D, Takeuchi J, Morimura T, Miyatake S I, Nakatsu S, Oda Y, Kikuchi H
机构信息
Department of Neurosurgery, Utano National Hospital, Kyoto, Japan.
出版信息
Br J Cancer. 1994 Apr;69(4):627-32. doi: 10.1038/bjc.1994.123.
Abstract
The mechanism by which tumour necrosis factor (TNF)-alpha increases the susceptibility of U87-MG human glioblastoma cells to lysis by natural killer (NK) cells was studied. Treatment with TNF-alpha (100 units ml-1) for 48 h enhanced the susceptibility of tumour cells to lysis by NK cells. Increased susceptibility to lysis was associated with enhanced expression of intercellular adhesion molecule 1 (ICAM-1) and HLA class I antigen. Antisense ICAM-1 oligonucleotide inhibited lysis by NK cells of TNF-alpha-treated tumour cells. In contrast, acid treatment following TNF-alpha treatment increased lysis by NK cells. These findings indicate that TNF-alpha treatment of glioblastoma cells increased their susceptibility to lysis by NK cells, since ICAM-1 up-regulation would have more profound effects on NK susceptibility than would HLA class I antigen up-regulation.
摘要
研究了肿瘤坏死因子（TNF）-α增加U87-MG人胶质母细胞瘤细胞对自然杀伤（NK）细胞裂解敏感性的机制。用TNF-α（100单位/毫升）处理48小时可增强肿瘤细胞对NK细胞裂解的敏感性。对裂解敏感性的增加与细胞间黏附分子1（ICAM-1）和HLA I类抗原表达的增强有关。反义ICAM-1寡核苷酸抑制了NK细胞对TNF-α处理的肿瘤细胞的裂解。相反，TNF-α处理后进行酸处理增加了NK细胞的裂解。这些发现表明，TNF-α处理胶质母细胞瘤细胞增加了它们对NK细胞裂解的敏感性，因为ICAM-1上调对NK敏感性的影响比HLA I类抗原上调更深远。
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