A novel approach for understanding the effects of interferons--a working hypothesis.
Experimental results accumulated during the last two decades prove that there are no mechanisms specific for interferon (IFN) action. Thus, IFN effects must be realized through the relatively limited number of metabolic pathways available for cell functions. Triggering the receptor system in association with membrane phospholipid breakdown, which plays an important role in signal transduction for a variety of biologically active substances, is suitable to explain generation of the pleiotropic IFN effects, too. Prevalence of one or the other of the "positive" and "negative" pathways of this signal transducing system depending on various known and up-to-now unknown factors may be responsible for the sometimes contradictory effects of IFNs.
D000818:Animals; D002118:Calcium / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D006152:Cyclic GMP / Q000502:physiology; D004075:Diglycerides / Q000502:physiology; D006801:Humans; D007295:Inositol Phosphates / Q000502:physiology; D007372:Interferons / Q000502:physiology*; D008954:Models, Biological; D011493:Protein Kinase C / Q000502:physiology; D011971:Receptors, Immunologic / Q000502:physiology*; D017471:Receptors, Interferon
D004075:Diglycerides; D007295:Inositol Phosphates; D011971:Receptors, Immunologic; D017471:Receptors, Interferon; D007372:Interferons; D011493:Protein Kinase C; D006152:Cyclic GMP; D002118:Calcium