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Defective tumoricidal capacity of macrophages from A/J mice. III. Genetic analysis of the macrophage defect.

作者信息

Boraschi D, Meltzer M S

出版信息

J Immunol. 1980 Mar;124(3):1050-3.

PMID:6987306
Abstract
摘要

相似文献

1
Defective tumoricidal capacity of macrophages from A/J mice. III. Genetic analysis of the macrophage defect.
J Immunol. 1980 Mar;124(3):1050-3.
2
Defective tumoricidal capacity of macrophages from A/J mice. II. Comparison of the macrophage cytotoxic defect of A/J mice with that of lipid A-unresponsive C3H/HeJ mice.A/J小鼠巨噬细胞的肿瘤杀伤能力缺陷。II. A/J小鼠巨噬细胞细胞毒性缺陷与脂质A无反应性C3H/HeJ小鼠的比较。
J Immunol. 1979 Apr;122(4):1592-97.
3
Defective tumoricidal capacity of macrophages from P/J mice: characterization of the macrophage cytotoxic defect after in vivo and in vitro activation stimuli.P/J 小鼠巨噬细胞的肿瘤杀伤能力缺陷：体内和体外激活刺激后巨噬细胞细胞毒性缺陷的特征
J Immunol. 1980 Aug;125(2):771-6.
4
Defective tumoricidal capacity of macrophages from A/J mice. I. Characterization of the macrophage cytotoxic defect after in vivo and in vitro activation stimuli.A/J小鼠巨噬细胞的肿瘤杀伤能力缺陷。I. 体内和体外激活刺激后巨噬细胞细胞毒性缺陷的特征
J Immunol. 1979 Apr;122(4):1587-91.
5
Defective tumoricidal capacity of macrophages from P/J mice: tumoricidal defect involves abnormalities in lymphokine-derived activation stimuli and in mononuclear phagocyte responsiveness.P/J小鼠巨噬细胞的肿瘤杀伤能力缺陷：肿瘤杀伤缺陷涉及淋巴因子衍生的激活刺激和单核吞噬细胞反应性的异常。
J Immunol. 1980 Aug;125(2):777-82.
6
Macrophage activation for tumor cytotoxicity: control of macrophage tumoricidal capacity by the LPS gene.巨噬细胞激活以实现肿瘤细胞毒性：LPS基因对巨噬细胞杀瘤能力的控制
J Immunol. 1978 Aug;121(2):543-8.
7
Macrophage function in tumor-bearing mice: tumoricidal and chemotactic responses of macrophages activated by infection with Mycobacterium bovis, strain BCG.荷瘤小鼠体内巨噬细胞的功能：经牛分枝杆菌卡介苗株感染激活的巨噬细胞的杀瘤和趋化反应
J Immunol. 1977 Jun;118(6):2176-81.
8
Characterization of genetic defects in macrophage tumoricidal capacity: identification of murine strains with abnormalities in secretion of cytolytic factors and ability to bind neoplastic targets.巨噬细胞杀肿瘤能力的遗传缺陷特征：具有溶细胞因子分泌异常和结合肿瘤靶标能力异常的小鼠品系的鉴定。
J Immunol. 1981 May;126(5):1843-7.
9
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。
J Immunol. 1981 Mar;126(3):1013-5.
10
Macrophage activation for tumor cytotoxicity: genetic variation in macrophage tumoricidal capacity among mouse strains.
Cell Immunol. 1979 Jun;45(1):188-94. doi: 10.1016/0008-8749(79)90375-7.

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Tumor progression stage and anatomical site regulate tumor-associated macrophage and bone marrow-derived monocyte polarization.肿瘤进展阶段和解剖部位调节肿瘤相关巨噬细胞和骨髓来源的单核细胞的极化。
Am J Pathol. 2010 Jun;176(6):2972-85. doi: 10.2353/ajpath.2010.090879. Epub 2010 Apr 29.
2
A/J mice are susceptible and C57BL/6 mice are resistant to Listeria monocytogenes infection by intragastric inoculation.通过胃内接种，A/J小鼠对单核细胞增生李斯特菌感染敏感，而C57BL/6小鼠具有抗性。
Infect Immun. 2003 Feb;71(2):682-9. doi: 10.1128/IAI.71.2.682-689.2003.
3
Phylogenetic variation and polymorphism at the toll-like receptor 4 locus (TLR4).
Toll样受体4基因座（TLR4）的系统发育变异和多态性。
Genome Biol. 2000;1(1):RESEARCH002. doi: 10.1186/gb-2000-1-1-research002. Epub 2000 Apr 27.
4
Differences in tumour necrosis factor productive ability among rodents.啮齿动物之间肿瘤坏死因子产生能力的差异。
Br J Cancer. 1984 Oct;50(4):471-8. doi: 10.1038/bjc.1984.203.
5
Phenotypic differentiation patterns of the human monocyte/macrophage system.人类单核细胞/巨噬细胞系统的表型分化模式
Histochem J. 1986 Aug;18(8):441-50. doi: 10.1007/BF01675337.
6
Lack of binding of bacterial lipopolysaccharide to mouse lung macrophages and restoration of binding by gamma interferon.细菌脂多糖与小鼠肺巨噬细胞的结合缺失以及γ干扰素对结合的恢复作用。
J Exp Med. 1985 Nov 1;162(5):1444-59. doi: 10.1084/jem.162.5.1444.
7
Inhibition of interferon-gamma-mediated activation in mouse macrophages treated with lipoarabinomannan.用脂阿拉伯甘露聚糖处理的小鼠巨噬细胞中γ-干扰素介导的激活的抑制作用
Clin Exp Immunol. 1990 Apr;80(1):141-8. doi: 10.1111/j.1365-2249.1990.tb06454.x.
8
Genetic control of natural resistance in mouse macrophages regulating intracellular Legionella pneumophila multiplication in vitro.小鼠巨噬细胞中天然抗性的遗传控制对体外嗜肺军团菌细胞内增殖的调节作用
Infect Immun. 1991 Jan;59(1):428-32. doi: 10.1128/iai.59.1.428-432.1991.