MODULATION OF THE ANTITUMOR EFFECT OF INTERFERON

干扰素（IFN）已被证明对肿瘤生长有深远的影响， 病毒复制和免疫反应。 这项研究涉及两个 IFN系统的重要机制。 第一 该机制涉及不同IFN的合作相互作用，当它们 被组合使用。 这种增强作用发生在小鼠和 当IFN-γ与IFN-α或IFN-β混合时， 混合物 IFN-α和IFN-β的表达不显示增强作用。 增强提供 IFN活性比预期水平高10至200倍以上 基于IFN的可加性。 这种IFN的巨大增加 已经注意到对于体内和体外抗肿瘤系统的活性， 以及体外抗病毒系统。 各种病毒、肿瘤和细胞 线将被使用。 这项研究将更仔细地量化 增强现象，试图阐明的机制， 发生增强，并评估可能的临床 应用程序. 第二种干扰素调节机制涉及干扰素作用的抑制剂 其由促分裂原刺激的小鼠和人白细胞产生。 这 抑制剂阻断抗病毒、抗细胞和免疫调节活性 的IFN。 本研究将采用批量生产和纯化的抑制剂 因此，它可以被表征并用于研究调制 以及控制IFN的抗肿瘤和抗病毒活性。

Interferon (IFN) has been shown to have a profound effect on tumor growth, viral replication, and the immune response. This study addresses two important mechanisms by which the IFN system is regulated. The first mechanism involves the cooperative interaction of different IFNs when they are employed in combination. This potentiation occurs for both mouse and human systems when IFN-Gamma is mixed with IFN-Alpha or IFN-Beta. Mixtures of IFN-Alpha and IFN-Beta do not show potentiation. Potentiation provides a 10- to more than 200-fold greater than expected level of IFN activity based on the additivity of the IFNs. This tremendous increase in IFN activity has been noted for both in vivo and in vitro antitumor systems as well as in vitro antiviral systems. A variety of viruses, tumors, and cell lines will be employed. This study will more carefully quantitate the potentiation phenomenon, seek to elucidate the mechanisms by which potentiaton occurs, and evaluate potentation for possible clinical application. The second mechanism of IFN regulation involves an inhibitor of IFN action which is produced by mitogen-stimulated mouse and human leukocytes. This inhibitor blocks the antiviral, anticellular, and immunoregulatory activity of IFN. This study will employ inhibitor produced and purified in bulk quantities so it may be characterized and employed to study the modulation and control of the antitumor and antiviral activities of IFN.