Regulation of Natural Killer Cytotoxicity by Escherichia coli‐Derived Human Interferon Gamma
Regulation of Natural Killer Cytotoxicity by Escherichia coli‐Derived Human Interferon Gamma
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大肠杆菌衍生的人干扰素γ对自然杀伤细胞毒性的调节
DOI：
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发表时间：
1986
影响因子：
3.7
通讯作者：
C. Platsoucas
中科院分区：
文献类型：
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作者：
C. Platsoucas
大肠杆菌衍生的人干扰素γ（IFN-γ）和E.比较了大肠杆菌衍生的人干扰素-μA（IFN-μA）或-μ2（IFN-μ2）增强自然杀伤（NK）细胞毒性的作用。当使用低浓度（小于10个抗病毒单位/ml）的干扰素时，使用相同数量的抗病毒单位的E。大肠杆菌来源的IFN-γ和E.大肠杆菌衍生的IFN-μA或IFN-μ2。比较它们增强NK的能力。E.大肠杆菌来源的IFN-γ在增强NK细胞对K562靶点的杀伤作用方面比大肠杆菌更有活性。大肠杆菌衍生的IFN-μA或IFN-μ2。这些实验中的抗病毒单位通过标准细胞病变效应试验使用水泡性口炎病毒（VSV）激发的人成纤维细胞（染色体21为三体）测定。然而，当这些干扰素以重量为基础（ng/ml）或以摩尔为基础进行比较时，它们增强NK对K562靶点的能力是相当的。这些干扰素增强NK的相对能力（当其浓度以抗病毒单位/ml表示时）的这些差异是由于其比活性（每mg干扰素的抗病毒单位）的约100倍差异。这些是1。8 × 106单位/mg;大肠杆菌衍生的IFN-γ，2. 0 × 108单位/mg;大肠杆菌来源的IFN-μA，和1. 8 × 108单位/mg;大肠杆菌来源的IFN-μ2。浓度高于10单位/毫升。所有这些干扰素显示出类似的增强NK的能力。对增强的动力学研究表明，在体外用E。对于增强NK针对来自造血人类肿瘤细胞系的靶标（K562，Daudi），需要将来自大肠杆菌的IFN-γ持续数小时。相反，α-干扰素在体外处理后能够显著地增加NK细胞的细胞毒性，时间较短（某些供体为30分钟或更短）。大肠杆菌来源的IFN-γ并不伴随着白细胞介素2（IL-2）的诱导产生，这表明1 L. IFN-γ-2不参与IFN-γ对NK细胞的增强作用，一种针对人IFN-γ的单克隆抗体阻断了E.大肠杆菌来源的IFN-γ和天然IFN-γ，但不被E.大肠杆菌来源的IFN-μA或葡萄球菌肠毒素A（SEA）。用该抗IFN-γ单克隆抗体预处理（37°C下14 h）效应细胞或将该抗体直接添加到15铬释放试验中对NK细胞毒性没有影响，表明组成型产生的IFN-γ不是维持NK细胞毒性所必需的。
The abilities of Escherichia coli‐ derived human interferon gamma (IFN‐γ) and E. coii‐ derived human interferon‐μA (IFN‐μA) or ‐μ2 (IFN‐μ2) to augment natural killer (NK) cytotoxicity were compared. When low concentrations (less than 10 antiviral units/ml) of interferons were used, and equal numbers of antiviral units of E. coli‐derived IFN‐γ and E. coli‐ derived IFN‐μA or IFN‐μ2. were compared for their ability to augment NK. E. coli‐derived IFN‐γ was found to be more active in augmenting NK against the K562targets, than E. coli‐ derived IFN‐μA or IFN‐μ2. Antiviral units in these experiments were determined by the standard cytopathic effect assay using vesicular stomatitis virus (VSV)‐challenged human fibroblasts, trisomic for chromosome 21. However, when these interferons were compared on a weight basis (ng/ml) or on a molar basis, their ability to augment NK against the K562 targets was comparable. These differences in the relative abilities of these interferons (when their concentrations were expressed in antiviral units/ml) to augment NK, were due to an approximately 100‐fold difference in their specific activities (antiviral units per mg of interferon). These were 1. 8 × 106 units/mg for E. coli‐derived IFN‐γ, 2. 0 × 108 units/mg for E. coli‐derived IFN‐μA,and 1. 8 × 108 units/mg for E. coli‐derived IFN‐μ2. At concentrations higher than 10 units/ml. all these interferons showed a similar ability to augment NK. Studies on the kinetics on the augmentation revealed that in vitro treatment with E. coli‐derived IFN‐γ for several hours was necessary for augmentation of NK against targets from haemopoietic human tumour cell lines (K562, Daudi). In contrast, alpha interferons were able to augment NK after treatment in vitro for significantly shorter periods (30 min or less with certain donors), Augmentation of NK cytotoxicity of human peripheral blood mononuclear leucocytes by E. coli‐derived IFN‐γ was not accompanied by the induction of interleukin 2 (IL‐2) production, suggesting that 1L. ‐2 is not involved in the augmentation of NK by 1FN‐γ, A monoclonal antibody specific for human IFN‐γ blocked augmentation of NK by E. coli‐derived IFN‐γ and natural IFN‐γ ‐ but not by E. coli‐derived IFN‐μA or staphylococcal enterotoxin A (SEA). Pretreatment (14 h at 37°C) of effector cells with this anti‐IFN‐γ monoclonal antibody or addition of this antibody directly into the 15chromium release assay had no effect on NK cytotoxicity, suggesting that constitutively produced IFN‐γ is not required for maintaining NK cytotoxicity.
葡萄球菌肠毒素 A 对人类白细胞的免疫调节：自然杀伤细胞的增强和抑制细胞的诱导。
影响因子：
4.3
作者：
Platsoucas,CD;Oleszak,EL;Good,RA
通讯作者：
Good,RA