SUMMARYPre-treatment of L cells with 750 units/ml of mouse interferon depressed the yield of interferon when the cells were treated with Newcastle disease virus (NDV). The refractory state persisted for more than 5 days. Nucleated fragments (karyoplasts) obtained by cytochalasin B-induced enucleation were made from such interferon pre-treated ceils; cells reconstituted from these karyoplasts produced less interferon in response to NDV than did ceils reconstituted from karyoplasts derived from untreated cells. The source of the enucleated cytoplasm (cytoplasts) used in the cellular reconstitutions did not affect the yields of interferon.Mammalian cells treated with a virus (e.g. Newcastle disease virus) or double-stranded RNA [e.g. poly(rI), poly(rC)] produce and secrete interferons, glycoproteins which interact with cells of the same or closely related species and produce in them an antiviral state (Lampson et al. I967; Field et al. I967; Vilcek & Kohase, I977). Production of interferon is dependent on cellular RNA and protein synthesis (Heller, 1963; Wagner, I964; Ho & Breinig, ~965; Youngner et al. 1965; Johnston & Burke, I973). Recently, reconstituted cells capable of interferon synthesis have been produced by means of cellular enucleation and reconstruction techniques (Burke & Veomett, I977). Such studies have confirmed previous conclusions by showing that the production of interferon is initially dependent upon the presence of a nucleus and that enucleated cells (cytoplasts) continue the synthesis of interferon if the cells were producing it prior to enucleation.Cells which have been treated with high concentrations of interferon produce relatively small amounts of interferon upon subsequent stimulation with an interferon inducer (Lockart, I963; Stewart et al. ~970. This property of interferon pre-treatment has been called 'blocking' (Colby, I977). The degree and duration of the inhibition of interferon synthesis is dependent upon the concentration of interferon used in the pre-treatment and the conditions of cell growth (Paucker & Boxaca, 1967). Although the factor(s) which causes the blocking reaction appears to co-purify with interferon (Golgher & Paucker, I973), the two activities -blocking and ability to induce the antiviral state -may be separable entities (e.g. Stringfellow, t976, ~977)-Little has been reported concerning the mechanism(s) which inhibit interferon synthesis in 'blocked' cells. For example, the antiviral state could be the factor responsible, with the inhibition of interferon synthesis resulting from the inability of the inducing virus to make the intracellular 'inducer' of interferon (Bausek & Merigan, I97o). Alternatively, there may be a block in the transcription of the interferon genes or translation of the interferon message or in some other step involved in interferon production.We have investigated the refractory state for interferon synthesis in cells 'blocked' by interferon pre-treatment, using cells reconstituted from nucleated fragments (karyoplasts) and enucleated fragmen...
SUMMARYL cells grown for 18 to 22 months in the presence of interferon (IEN) retained their sensitivity to the antiviral effect of IFN but were less sensitive to cell growth inhibition b'y IFN. Moreover, the parental and variant lines became hyporesponsive (i.e. less responsive to virus induction of IFN) with different kinetics after IFN treatment.
The interferon (IFN)-dependent induction of two double-stranded RNA-dependent enzymes was examined in L cells and an L-cell variant (WDIFN) which is highly resistant to the inhibitory effects of IFN on cellular multiplication. IFN, in a concentration-dependent manner, inhibited the multiplication of parental L cells and induced increased levels of the double-stranded RNA-dependent enzymes in parental L cells. Although WDIFN cells were resistant to the antiproliferative effects of IFN, the cells responded to IFN by increasing their levels of the double-stranded RNA-dependent enzymes. However, the level of activity of each enzyme was lower in the WDIFN line than the parental line when both lines were treated with similar concentrations of IFN. The reduced response of the WDIFN line was not the result of the line being a heterogeneous population of cells nor of IFN being more unstable in the presence of WDIFN cells. In addition there was no evidence that WDIFN cells produced a mitogenic factor that could overcome the antiproliferative effects of IFN, nor that sodium butyrate could increase the sensitivity of WDIFN cells to the antiproliferative effects of IFN.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.