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巨噬细胞可诱导豚鼠白血病细胞发生抗体依赖性细胞停滞,但不会导致其裂解。

Macrophages induce antibody-dependent cytostasis but not lysis in guinea pig leukaemic cells.

作者信息

Lawson A D, Stevenson G T

出版信息

Br J Cancer. 1983 Aug;48(2):227-37. doi: 10.1038/bjc.1983.178.

DOI:10.1038/bjc.1983.178
PMID:6882663
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2011445/
Abstract

Guinea pig and mouse peritoneal macrophages formed antibody-dependent rosettes with guinea pig L2C leukaemic cells, but were unable either to phagocytose the cells or to kill them extracellularly as judged by the retention of 51Cr. Macrophages previously activated by BCG in vivo also failed to exhibit phagocytosis or cytoxicity towards the antibody-coated cells. These failures could not be attributed to deficient function of the macrophages nor to antigenic modulation of the L2C cells. The antibodies involved were capable of mediating lysis by complement, and ADCC by human leukocytes. However macrophages were cytostatic to antibody-coated L2C cells in that uptake of 3H-thymidine or 3H-deoxycytidine was abruptly and in some cases completely inhibited upon cell contact being established. Antigenic modulation which had proceeded sufficiently to protect against lysis by complement did not protect against cytostasis. Syngeneic macrophages had greater cytostatic activity than did allogeneic or xenogeneic. Macrophage activation by BCG did not result in significantly increased cytostasis. A univalent antibody derivative Fab/c was also capable of mediating cytostatis by the macrophages.

摘要

豚鼠和小鼠的腹腔巨噬细胞与豚鼠L2C白血病细胞形成抗体依赖性玫瑰花结,但无论是通过吞噬细胞还是通过51Cr的保留来判断细胞外杀伤,它们都无法做到。先前在体内被卡介苗激活的巨噬细胞对抗体包被的细胞也未表现出吞噬作用或细胞毒性。这些失败不能归因于巨噬细胞功能缺陷或L2C细胞的抗原调变。所涉及的抗体能够介导补体裂解以及人白细胞的抗体依赖性细胞介导的细胞毒性作用(ADCC)。然而,巨噬细胞对抗体包被的L2C细胞具有细胞生长抑制作用,因为一旦建立细胞接触,3H-胸腺嘧啶核苷或3H-脱氧胞苷的摄取就会突然且在某些情况下完全受到抑制。足以防止补体裂解的抗原调变并不能防止细胞生长抑制。同基因巨噬细胞比异基因或异种巨噬细胞具有更强的细胞生长抑制活性。卡介苗激活巨噬细胞并未导致细胞生长抑制作用显著增强。单价抗体衍生物Fab/c也能够介导巨噬细胞的细胞生长抑制作用。

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引用本文的文献

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Mechanisms of tumour cell escape encountered in treating lymphocytic leukaemia with anti-idiotypic antibody.用抗独特型抗体治疗淋巴细胞白血病时遇到的肿瘤细胞逃逸机制。
Br J Cancer. 1984 May;49(5):547-57. doi: 10.1038/bjc.1984.88.
2
Further studies on the differences in cytotoxicity of human peripheral blood monocytes and bronchoalveolar macrophages for cultured human lung cells.关于人外周血单核细胞和支气管肺泡巨噬细胞对培养的人肺细胞细胞毒性差异的进一步研究。
Cancer Immunol Immunother. 1985;19(1):62-7. doi: 10.1007/BF00199314.
3
Effects of L2C leukemia on macrophage-mediated responses.L2C白血病对巨噬细胞介导反应的影响。
Cancer Immunol Immunother. 1987;25(2):75-80. doi: 10.1007/BF00199944.

本文引用的文献

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Opsonization of cells by isoantibody in vitro.体外同种抗体对细胞的调理作用。
Nature. 1963 Apr 6;198:10-2. doi: 10.1038/198010a0.
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Artificial binding of macrophages to syngeneic cells elicits cytostasis but not cytolysis.巨噬细胞与同基因细胞的人工结合会引发细胞停滞,但不会导致细胞溶解。
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Studies on the antibody-dependent cell-mediated cytotoxicity (ADCC) of thioglycollate-stimulated and BCG-activated peritoneal macrophages.巯基乙酸盐刺激和卡介苗激活的腹腔巨噬细胞的抗体依赖性细胞介导的细胞毒性(ADCC)研究
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9
Evidence for a multistep mechanism of cytolysis by BCG-activated macrophages: the interrelationship between the capacity for cytolysis, target binding, and secretion of cytolytic factor.卡介苗激活的巨噬细胞进行细胞溶解的多步骤机制的证据:细胞溶解能力、靶细胞结合及细胞溶解因子分泌之间的相互关系。
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10
The ADCC capacity of macrophages from C3H/HeJ and A/J mice can be augmented by BCG.卡介苗可增强C3H/HeJ和A/J小鼠巨噬细胞的抗体依赖细胞介导的细胞毒性(ADCC)能力。
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