A species of human alpha interferon that lacks the ability to boost human natural killer activity.
A species of human alpha interferon that lacks the ability to boost human natural killer activity.
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一种人类α干扰素，缺乏增强人类自然杀伤活性的能力。
DOI：
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发表时间：
1984
影响因子：
11.1
通讯作者：
S. Pestka
中科院分区：
文献类型：
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作者：
J. Ortaldo;R. Herberman;C. Harvey;P. Osheroff;Y. C. Pan;B. Kelder;S. Pestka
大多数种类的重组白细胞干扰素（IFN-α A、IFN-α B、IFN-α C、IFN-α D、IFN-α F、IFN-α I和IFN-α K）在以1 - 80单位/ml的浓度处理细胞2小时后能够增强人自然杀伤（NK）活性。相反，发现重组人IFN-α J在细胞暴露于高达10，000单位/ml的浓度2小时后不能增强NK活性。IFN-α J不能增强NK活性是不完全的，因为在将细胞暴露于高浓度IFN-α J（10，000单位/ml）18小时后，观察到细胞溶解的增强。IFN-α J似乎与NK细胞上的IFN受体相互作用，因为发现它干扰其他种类的IFN-α对NK活性的增强。与其增强NK活性的能力不足相反，IFN-α J具有有效的抗病毒和抗增殖活性。这些生物活性的这种广泛解离以前在任何其它天然或重组IFN种类中未观察到。因此，这种IFN物种可能是有用的，用于评估各种生物活性对IFN的治疗效果的相对重要性，用于理解结构-功能关系，以及用于确定与IFN的各种生物效应相关的生化途径。
Most species of recombinant leukocyte interferons (IFN-alpha A, -alpha B, -alpha C, -alpha D, -alpha F, -alpha I, and -alpha K) were capable of boosting human natural killer (NK) activity after a 2-hr treatment of cells at a concentration of 1-80 units/ml. In contrast, recombinant human IFN-alpha J was found to be incapable of augmenting NK activity after exposure of cells for 2 hr to concentrations as high as 10,000 units/ml. This inability of IFN-alpha J to boost NK activity was not complete because, after exposure of cells to a high concentration of IFN-alpha J (10,000 units/ml) for 18 hr, boosting of cytolysis was observed. IFN-alpha J appeared to interact with receptors for IFN on NK cells since it was found to interfere with the boosting of NK activity by other species of IFN-alpha. In contrast to its deficient ability to augment NK activity, IFN-alpha J has potent antiviral and antiproliferative activities. Such extensive dissociation of these biological activities has not been observed previously with any other natural or recombinant IFN species. Thus, this IFN species may be useful for evaluating the relative importance of various biological activities on the therapeutic effects of IFN, for understanding structure-function relationships, and for determining the biochemical pathways related to the various biological effects of IFN.