Immune and virus-induced interferons may activate cells by different derepressional mechanisms.
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.
D000818:Animals; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D006801:Humans; D007369:Interferon Inducers / Q000494:pharmacology*; D007372:Interferons / Q000494:pharmacology*; D008214:Lymphocytes / Q000502:physiology; D011506:Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D014762:Viral Interference / Q000187:drug effects*; D014777:Virus Diseases / Q000276:immunology
D007369:Interferon Inducers; D011506:Proteins; D012333:RNA, Messenger; D007372:Interferons; D003513:Cycloheximide