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诺卡氏菌细胞壁骨架刺激的T细胞产生的一种因子增强小鼠淋巴因子激活的杀伤细胞诱导作用。

Augmentation of murine lymphokine-activated killer cell induction by a factor produced by Nocardia rubra cell wall skeleton-stimulated T cells.

作者信息

Kawase I, Shirasaka T, Ikeda T, Hara H, Tanio Y, Watanabe M, Saito S, Masuno T, Kishimoto S, Yamamura Y

机构信息

Third Department of Internal Medicine, Osaka University Medical School.

出版信息

Jpn J Cancer Res. 1989 Nov;80(11):1098-105. doi: 10.1111/j.1349-7006.1989.tb02265.x.

DOI:10.1111/j.1349-7006.1989.tb02265.x
PMID:2481664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5917909/
Abstract

Four-hour exposure of C3H/HeN mouse spleen cells to Nocardia rubra cell wall skeleton (N-CWS) before 4-day culture with a suboptimal dose of human recombinant interleukin 2 (rIL 2) augmented the induction of lymphokine-activated killer (LAK) cell activity, whereas the treatment with N-CWS alone induced no cytotoxicity. In accordance with this, the IL 2 binding activity of spleen cells was augmented by combined stimulation with N-CWS and rIL 2. The augmented cytotoxicity was mediated by Thy-1.2+, Lyt-1.1-, Lyt-2.1- and asialo GM1+ cells. Cell cultures in diffusion chambers revealed that N-CWS-treated spleen cells produced a LAK cell induction-helper factor (LAK-helper factor, LHF) when cultured with rIL 2. The LHF production required Thy-1.2+, Lyt-1.1+, Lyt-2.1+ and asialo GM1- cells, and the coexistence of unstimulated accessory cells was also essential for the LHF production. Cells responding to both LHF and rIL 2 to generate LAK activity were Thy-1.2-, Lyt-1.1-, Lyt-2.1- and asialo GM1+. The culture fluid of spleen cells stimulated with both N-CWS and rIL 2 contained no tumor necrosis factor (TNF) activity, and the additional stimulation with N-CWS caused no production of either IL 2 or interferon (IFN). Murine recombinant interleukin 1 alpha (Mu-rIL 1 alpha) could not replace the augmentative effect of N-CWS on LAK cell induction. These results suggest that in the presence of rIL 2, N-CWS stimulates murine T cells to produce LHF that is probably distinct from IL 1, IL 2, TNF and IFN.

摘要

在用次优剂量的人重组白细胞介素2(rIL-2)进行4天培养之前,将C3H/HeN小鼠脾细胞暴露于红色诺卡氏菌细胞壁骨架(N-CWS)4小时,可增强淋巴因子激活的杀伤(LAK)细胞活性的诱导,而单独用N-CWS处理则不诱导细胞毒性。与此一致的是,N-CWS和rIL-2联合刺激可增强脾细胞的IL-2结合活性。增强的细胞毒性由Thy-1.2 +、Lyt-1.1 -、Lyt-2.1 -和无唾液酸GM1 +细胞介导。扩散小室中的细胞培养显示,用rIL-2培养时,经N-CWS处理的脾细胞产生了一种LAK细胞诱导辅助因子(LAK辅助因子,LHF)。LHF的产生需要Thy-1.2 +、Lyt-1.1 +、Lyt-2.1 +和无唾液酸GM1 -细胞,未刺激的辅助细胞的共存对LHF的产生也至关重要。对LHF和rIL-2均有反应以产生LAK活性的细胞是Thy-1.2 -、Lyt-1.1 -、Lyt-2.1 -和无唾液酸GM1 +。用N-CWS和rIL-2刺激的脾细胞培养液中不含肿瘤坏死因子(TNF)活性,用N-CWS额外刺激不会导致IL-2或干扰素(IFN)的产生。小鼠重组白细胞介素1α(Mu-rIL-1α)不能替代N-CWS对LAK细胞诱导的增强作用。这些结果表明,在rIL-2存在的情况下,N-CWS刺激小鼠T细胞产生可能不同于IL-1、IL-2、TNF和IFN的LHF。

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引用本文的文献

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本文引用的文献

1
The role of interleukin-2 (IL-2) in the differentiatin of cytotoxic T cells: the effect of monoclonal anti-IL-2 antibody and absorption with IL-2 dependent T cell lines.白细胞介素-2(IL-2)在细胞毒性T细胞分化中的作用:单克隆抗IL-2抗体的作用及用IL-2依赖型T细胞系进行吸附的效果
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Interleukin 2 induces gamma-interferon production: participation of macrophages and NK-like cells.白细胞介素2诱导γ-干扰素生成:巨噬细胞和自然杀伤样细胞的参与
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Induction of a tumor necrosis factor-like activity by Nocardia rubra cell wall skeleton.红色诺卡氏菌细胞壁骨架诱导肿瘤坏死因子样活性
Cancer Res. 1987 Apr 1;47(7):1785-92.
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Combination immunotherapy for cancer: synergistic antitumor interactions of interleukin-2, alfa interferon, and tumor-infiltrating lymphocytes.癌症联合免疫疗法:白细胞介素-2、α干扰素和肿瘤浸润淋巴细胞的协同抗肿瘤相互作用
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Synergistic antitumor effects of immunotherapy with recombinant interleukin-2 and recombinant tumor necrosis factor-alpha.重组白细胞介素-2与重组肿瘤坏死因子-α免疫疗法的协同抗肿瘤作用
Cancer Res. 1988 Jul 15;48(14):4011-7.
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Combined therapy of mice bearing a lymphokine-activated killer-resistant tumor with recombinant interleukin 2 and an antitumor monoclonal antibody capable of inducing antibody-dependent cellular cytotoxicity.用重组白细胞介素2和一种能够诱导抗体依赖性细胞毒性的抗肿瘤单克隆抗体对携带抗淋巴因子激活的杀伤细胞肿瘤的小鼠进行联合治疗。
Cancer Res. 1988 Mar 1;48(5):1173-9.
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J Immunol. 1989 Apr 1;142(7):2307-13.