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免疫和病毒诱导的干扰素可能通过不同的去抑制机制激活细胞。

Immune and virus-induced interferons may activate cells by different derepressional mechanisms.

作者信息

Dianzani F, Zucca M, Scupham A, Georgiades J A

出版信息

Nature. 1980 Jan 24;283(5745):400-2. doi: 10.1038/283400a0.

Abstract

Virus-induced interferon (VIF), and immune interferon (IIF) produced by lymphocytes following activation by various mitogens (phytohaemagglutinin, concanavalin A, staphlococcal enterotoxin A) or by specific antigenic stimulation (tuberculin, bacterial toxoids, and viral antigens) show important functional differences. These include different antitumour and immunoregulatory activities and differential inhibition of activity by mercaptoethanol. Another important difference has recently been shown: cells treated with IIF acquire the antiviral state much more slowly than those treated with VIF. This may be due to (1) difference in cellular receptors, (2) presence of an inhibitor of antiviral activity in the IIF preparations, or (3) a different mechanism of activation of the antiviral state by the two types of interferon. The first two hypotheses seem unlikely, since (1) no difference between cell association by the two types of interferon has been detected, and (2) the presence of the slow acting IIF preparation did not inhibit the rapid activation by VIF. The present study shows that the different kinetics of induction of the antiviral state result from a major difference in the mechanism by which IIF and VIF activate cells.

摘要

病毒诱导的干扰素(VIF)以及淋巴细胞在被各种促有丝分裂原(植物血凝素、刀豆球蛋白A、葡萄球菌肠毒素A)激活后或被特异性抗原刺激(结核菌素、细菌类毒素和病毒抗原)后产生的免疫干扰素(IIF)表现出重要的功能差异。这些差异包括不同的抗肿瘤和免疫调节活性,以及巯基乙醇对活性的不同抑制作用。最近还发现了另一个重要差异:用IIF处理的细胞获得抗病毒状态的速度比用VIF处理的细胞慢得多。这可能是由于:(1)细胞受体的差异;(2)IIF制剂中存在抗病毒活性抑制剂;或(3)两种类型的干扰素激活抗病毒状态的机制不同。前两个假设似乎不太可能,因为:(1)未检测到两种类型的干扰素在细胞结合方面存在差异;(2)作用缓慢的IIF制剂的存在并未抑制VIF的快速激活。本研究表明,抗病毒状态诱导动力学的差异是由IIF和VIF激活细胞的机制的主要差异所致。

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