Intracellular human gamma-interferon triggers an antiviral state in transformed murine L cells.
Interaction of human gamma-interferon (IFN-gamma) with a cell-surface receptor is known to be essential for the cell to become resistant to viral infection. Here we demonstrate that IFN-gamma, when present inside the cell, is also capable of inducing a permanent antiviral state. Mouse cells transformed with a truncated human cDNA encoding a mature IFN-gamma protein lacking the signal peptide accumulate high levels of intracellular human IFN-gamma. Not only do these cells acquire a permanent resistance to viral infection, they also exhibit all the biochemical characteristics normally observed after exposure to exogenous IFN. The observed loss of species specificity normally associated with IFN-gamma suggests that this restriction is strictly dependent on the interaction of the molecule with the cell-surface receptor.
D015088:2',5'-Oligoadenylate Synthetase / Q000235:genetics; D000818:Animals; D002460:Cell Line; D004262:DNA Restriction Enzymes; D005796:Genes; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology* / Q000494:pharmacology; D007739:L Cells / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D051379:Mice; D011991:Receptors, Virus / Q000502:physiology*
D011991:Receptors, Virus; D007371:Interferon-gamma; D015088:2',5'-Oligoadenylate Synthetase; D004262:DNA Restriction Enzymes