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CD18/CD54(+CD102)、CD2/CD58途径非依赖性的淋巴因子激活的杀伤细胞(LAK细胞)对胶质母细胞瘤细胞系T98G和U373MG的杀伤作用

CD18/CD54(+CD102), CD2/CD58 pathway-independent killing of lymphokine-activated killer (LAK) cells against glioblastoma cell lines T98G and U373MG.

作者信息

Komatsu F, Kajiwara M

机构信息

Blood Transfusion Service, School of Medicine, Tokyo Medical and Dental University, Japan.

出版信息

Oncol Res. 2000;12(1):17-24. doi: 10.3727/000000001108747408.

DOI:10.3727/000000001108747408
PMID:11061342
Abstract

For natural killer cell-mediated cytolysis (NK-lysis) and lymphokine-activated killer cell-mediated cytolysis (LAK-lysis), the co-stimulatory signals of CD18/CD54(+CD102) and CD2/CD58 pathways are essential. However, in this report, we describe a LAK-lysis that does not depend upon these two pathways. The killed cells were glioblastoma cell lines T98G and U373MG. The LAK cells were induced from peripheral blood lymphocytes in the presence of interleukin-2. 1) The T98G and U373MG did not express CD54 or CD102, but expressed CD58. 2) However, when they were pretreated with an anti-CD58 (TS2/9), the LAK-lysis was not blocked. 3) The LAK-lysis was markedly inhibited by pretreating with Concanamycin A and slightly inhibited by treating with antitumor necrosis factor-related apoptosis-inducing ligand (anti-TRAIL) antibody. 4) Nineteen percent of the LAK cells adhered to the T98G. The adhered LAK cells killed it. But nonadherent LAK cells could not kill the T98G or U373MG but killed lymphoblastoma cell lines Raji and NALM-6. These findings suggested that this type of the LAK-lysis might not depend upon the CD18/CD54(+CD102) pathway or CD2/CD58 pathway. The effector cells that killed the T98G and U373MG might not always be the same as the effector cells that killed the other cell lines. The LAK cells contain several subsets, and one of the subsets might kill these two target cell lines.

摘要

对于自然杀伤细胞介导的细胞溶解作用(NK 细胞溶解)和淋巴因子激活的杀伤细胞介导的细胞溶解作用(LAK 细胞溶解),CD18/CD54(+CD102)和 CD2/CD58 途径的共刺激信号至关重要。然而,在本报告中,我们描述了一种不依赖于这两条途径的 LAK 细胞溶解作用。被杀伤的细胞是胶质母细胞瘤细胞系 T98G 和 U373MG。LAK 细胞是在白细胞介素-2 存在的情况下从外周血淋巴细胞诱导产生的。1)T98G 和 U373MG 不表达 CD54 或 CD102,但表达 CD58。2)然而,当用抗 CD58(TS2/9)对它们进行预处理时,LAK 细胞溶解作用并未被阻断。3)用 concanamycin A 预处理可显著抑制 LAK 细胞溶解作用,用抗肿瘤坏死因子相关凋亡诱导配体(抗 TRAIL)抗体处理则有轻微抑制作用。4)19%的 LAK 细胞黏附于 T98G。黏附的 LAK 细胞将其杀伤。但未黏附的 LAK 细胞不能杀伤 T98G 或 U373MG,却能杀伤淋巴瘤细胞系 Raji 和 NALM-6。这些发现表明,这种类型的 LAK 细胞溶解作用可能不依赖于 CD18/CD54(+CD102)途径或 CD2/CD58 途径。杀伤 T98G 和 U373MG 的效应细胞可能并不总是与杀伤其他细胞系的效应细胞相同。LAK 细胞包含几个亚群,其中一个亚群可能杀伤这两种靶细胞系。

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