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细菌脂多糖增强小鼠重组干扰素-γ对Lewis肺癌的抗肿瘤效力。

Augmentation by bacterial lipopolysaccharide of antitumor potency of murine recombinant interferon-gamma against Lewis lung adenocarcinoma.

作者信息

Nagao S, Sato K, Ogawa H, Osada Y

出版信息

Jpn J Cancer Res. 1986 Feb;77(2):212-8.

PMID:3082834
Abstract

Stimulation by recombinant murine interferon-gamma (rMuIFN-gamma) of host defenses against the growth of Lewis lung adenocarcinoma, cell line 3LL, in the lung was examined. 3LL cells were resistant to in vitro antiproliferative activities of rMuIFN-gamma. On the other hand, rMuIFN-gamma augmented the killer activities of the non-adherent population of spleen cells and peripheral blood mononuclear cells (PBMC) in vivo, and the IFN also stimulated the cytostatic activities of peritoneal and splenic macrophages, but not alveolar macrophages. The combination of rMuIFN-gamma with LPS synergistically activated macrophages from the lung, as well as the peritoneal cavity and the spleen, to become both cytostatic and cytolytic against 3LL cells. The macrophages activated in vitro by simultaneous incubation with these agents markedly suppressed the growth of 3LL cells in vivo. The growth in the lung of 3LL cells implanted iv was significantly (P less than 0.05) suppressed by combination therapy with rMuIFN-gamma and LPS, but not by either agent alone. These results indicate that the potency of rMuIFN-gamma action against 3LL cells can be augmented by combination with LPS, mainly through synergistic macrophage activation.

摘要

研究了重组鼠γ干扰素(rMuIFN-γ)对宿主抵抗Lewis肺癌3LL细胞系在肺部生长的防御机制的刺激作用。3LL细胞对rMuIFN-γ的体外抗增殖活性具有抗性。另一方面,rMuIFN-γ在体内增强了脾细胞和外周血单核细胞(PBMC)非贴壁群体的杀伤活性,并且该干扰素还刺激了腹腔和脾巨噬细胞的细胞抑制活性,但未刺激肺泡巨噬细胞。rMuIFN-γ与LPS联合使用可协同激活来自肺以及腹腔和脾脏的巨噬细胞,使其对3LL细胞具有细胞抑制和细胞溶解作用。通过与这些试剂同时孵育在体外激活的巨噬细胞显著抑制了3LL细胞在体内的生长。静脉注射植入的3LL细胞在肺部的生长通过rMuIFN-γ和LPS联合治疗得到显著(P<0.05)抑制,但单独使用任何一种试剂均无此效果。这些结果表明,rMuIFN-γ与LPS联合使用可增强其对3LL细胞的作用效力,主要是通过协同激活巨噬细胞实现的。

相似文献

1
Augmentation by bacterial lipopolysaccharide of antitumor potency of murine recombinant interferon-gamma against Lewis lung adenocarcinoma.细菌脂多糖增强小鼠重组干扰素-γ对Lewis肺癌的抗肿瘤效力。
Jpn J Cancer Res. 1986 Feb;77(2):212-8.
2
Augmentation by priming with interferon-gamma of the binding of a muramyl dipeptide derivative to macrophages resulting in synergistic macrophage activation.用γ-干扰素预处理增强胞壁酰二肽衍生物与巨噬细胞的结合,从而导致巨噬细胞的协同激活。
Jpn J Cancer Res. 1987 Jan;78(1):80-6.
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Effect of recombinant tumor necrosis factor on tumoricidal activation of murine macrophages: synergism between tumor necrosis factor and gamma-interferon.重组肿瘤坏死因子对小鼠巨噬细胞杀瘤活性的影响:肿瘤坏死因子与γ干扰素之间的协同作用。
Cancer Res. 1987 Nov 15;47(22):5868-74.
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Synergistic induction of cytotoxicity in macrophages by murine interferon-gamma and biological response modifiers derived from microorganisms.小鼠干扰素-γ与微生物衍生的生物反应调节剂协同诱导巨噬细胞产生细胞毒性。
Cancer Immunol Immunother. 1986;23(1):41-5. doi: 10.1007/BF00205553.
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Interferon-gamma synergizes with tumor necrosis factor and with interleukin 1 and requires the presence of both monokines to induce antitumor cytotoxic activity in macrophages.γ干扰素与肿瘤坏死因子以及白细胞介素1协同作用,并且需要两种单核因子同时存在才能诱导巨噬细胞产生抗肿瘤细胞毒性活性。
J Immunol. 1987 Dec 15;139(12):4096-101.
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Gamma interferon cooperates with lipopolysaccharide to activate mouse splenic macrophages to an antihistoplasma state.γ干扰素与脂多糖协同作用,将小鼠脾脏巨噬细胞激活至抗组织胞浆菌状态。
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Interferon-gamma or BCG restores the responsiveness of mouse lung macrophages to lipopolysaccharide.γ干扰素或卡介苗可恢复小鼠肺巨噬细胞对脂多糖的反应性。
Tokai J Exp Clin Med. 1986;11 Suppl:89-96.
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Inhibition of murine renal carcinoma pulmonary metastases by systemic administration of interferon gamma: mechanism of action and potential for combination with interleukin 4.通过全身给予γ干扰素抑制小鼠肾癌肺转移:作用机制及与白细胞介素4联合应用的潜力
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Restoration of lipopolysaccharide-mediated cytotoxic macrophage induction in C3H/HeJ mice by interferon-gamma or a calcium ionophore.通过γ干扰素或钙离子载体恢复C3H/HeJ小鼠中脂多糖介导的细胞毒性巨噬细胞诱导作用。
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Lipid A-associated proteins provide an alternate "second signal" in the activation of recombinant interferon-gamma-primed, C3H/HeJ macrophages to a fully tumoricidal state.脂多糖A相关蛋白在将重组γ干扰素预处理的C3H/HeJ巨噬细胞激活至完全杀瘤状态的过程中提供了另一种“第二信号”。
J Immunol. 1987 Dec 1;139(11):3697-702.

引用本文的文献

1
Synergistic induction of cytotoxicity in macrophages by murine interferon-gamma and biological response modifiers derived from microorganisms.小鼠干扰素-γ与微生物衍生的生物反应调节剂协同诱导巨噬细胞产生细胞毒性。
Cancer Immunol Immunother. 1986;23(1):41-5. doi: 10.1007/BF00205553.
2
Inhibition of spontaneous pulmonary metastases of Lewis lung carcinoma by oral treatment with Respivax and Broncho-Vaxom.通过口服Respivax和支气管疫苗抑制Lewis肺癌的自发性肺转移。
Cancer Immunol Immunother. 1991;33(5):307-13. doi: 10.1007/BF01756595.