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.
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