MODULATION OF THE ANTITUMOR EFFECT OF INTERFERON

干扰素已被证明对肿瘤生长有深远的影响， 病毒复制和免疫反应。这项研究涉及两个问题 干扰素系统调节的重要机制。第一 机制涉及不同IFN在它们之间的协作交互 是联合雇佣的。这种增强作用在小鼠和 当干扰素-伽玛与干扰素-α或干扰素-β混合时，对人体系统的影响。混合物 干扰素-α和干扰素-β未表现出增强作用。增强功能可提供 干扰素活性水平比预期高出10到200倍 基于IFN的可加性。干扰素的这种巨大增长 已经注意到体内和体外抗肿瘤系统的活性为 以及体外抗病毒系统。各种病毒、肿瘤和细胞 线路将会被使用。这项研究将更仔细地量化 增强现象，试图阐明其机制。 发生潜伏期，并评估可能的临床潜势 申请。 干扰素调节的第二种机制涉及干扰素作用的抑制物。 它是由丝裂原刺激的小鼠和人类白细胞产生的。这 抑制剂阻断了抗病毒、抗细胞和免疫调节活性 干扰素。这项研究将使用批量生产和纯化的缓蚀剂 量，因此它可以被刻画并用于研究调制 和控制干扰素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.