The role of the T3/antigen receptor complex is summarized by the diagram presented in Figure 4. Signals transmitted through T3/Ti activate a phosphodiesterase. This enzyme acts on its substrate PIP2 to generate two important mediators, IP3 and diacylglycerol. IP3 mobilizes calcium from bound intracellular stones. This increase in [Ca2+]i is one intracellular signal which, in conjunction with others, induces expression of lymphokine genes by influencing pretranslational, presumably transcriptional, events. Several problems remain. Which of the five molecules in the T3/Ti complex serves as the effector molecule in the transmembrane signaling process is not known. Which molecules serve to link T3/Ti to the phosphodiesterase enzyme is under investigation. The role diacylglycerol protein kinase C and other mediators play in signalling activation is not established. Finally, for those events occurring after the early events pictured in Figure 4 that result in gene activation, the sequence is a black box. Approaches to address each of these questions are available, and answers should be forthcoming.
In 1965 Wheelock reported that phytohemagglutinin could induce from human leukocytes an interferon-like virus inhibitor [1]. This substance, which turned out to be interferon-gamma (IFN-gamma), has been the subject, directly or indirectly, of thousands of scientific publications since that initial report. Past research has led to the general conclusion that IFN-gamma is much more than an interferon in that it has broader effects on the various arms of the immune system than most any other lymphokine or cytokine. In this review we discuss the effects of IFN-gamma on the various cell lineages of the immune system, focusing on the biology of its actions. In addition, we summarize research focused on the consequences of introducing IFN-gamma cDNA into tumor cells, aberrant IFN-gamma production in transgenic animals, and inhibition of IFN-gamma effects by knocking out either the IFN-gamma gene itself or the IFN-gamma receptor gene.
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