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Results for “Type I interferon”

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At least 19 recordsLinked to original sources
PubMed1992

[Interferon type I in protective body reactions in an experimental Klebsiella infection].

The study on mice with experimental generalized Klebsiella infection, carried out with the use of microbiologic, immunologic and pathomorphologic methods, revealed that the intraperitoneal injection of type I interferon into the animals prevented their death and led to the rapid elimination of the infective agent from their body, enhanced the phagocytic and metabolic activity of polymorphonuclear lymphocytes of their peritoneal exudate, decreased the manifestation of microcirculatory and dystrophic changes in the parenchyma of their internal organs.

Animals↗
PubMed1986

[Effect of interferon type I on the in vivo persistence of Salmonella typhimurium].

The influence of type I interferon on the persistence of S. typhimurium in the body of mice has been studied. The injection of the preparation of interferon has been shown to be conductive to the survival of the animals and to reduce the time of Salmonella persistence in the body. The injection of interferon enhances the phagocytic activity of macrophages in the peritoneal exudate of mice.

Animals↗
PubMed1991

[The protective action of interferon type I in experimental Salmonella infection].

The effect of interferon, type 1, on the course of Salmonella infection in mice has been studied. The study has shown that the injection of homologous interferon of type 1 leads to the rapid elimination of the infective agent from the blood and organs of infected mice. Morphological study has shown that the injection of the preparations of interferon of type 1 may diminish pathological changes in the organs of the infected animals and the coagulation system of their blood.

Animals↗
PubMed1992

[Proteins induced by various types of double-stranded RNA and interferon type I in human fibroblasts. Correlation with antiviral activity of the substances].

Protein induction by new antiviral preparations of dsRNAs (larifan, ridostin, rifastin and poly(A).poly(U)) and recombinant beta-interferon in human fibroblasts (M19) was studied. The common gene products: 88, 80, 68, 58, 56, 52, 50 and 26 kD were detected in the spectra of the induced cytoplasmic polypeptides. At the same time the sets of the induced proteins had individual distinctions in various preparations. Induction of the 56-kD protein was more essential in the action of dsRNAs than that of interferon. The antiviral activity of dsRNAs and interferon preparations correlated with a relative increase in the synthesis of proteins with molecular weights of 88, 80 and 58 kD. The study results are in agreement with the fact that the dsRNAs have interferon-independent pathways of antiviral action with participation of 56- and 58-kD protein genes.

Antiviral Agents↗
PubMed1991

Augmentation of cytotoxicity using combinations of interferons (types I and II), tumor necrosis factor-alpha, and tamoxifen in MCF-7 cells.

The cytotoxic effect of a combination of interferons (type I and II) and tumor necrosis factor (TNF), with an antiestrogenic drug, tamoxifen (TAM), was investigated in the estrogen receptor positive human breast carcinoma cell line, MCF-7. Cytotoxicity was measured by the MTT assay. In an attempt to define the molecular basis for the interaction between the interferons (IFNs) and TNF or any one of the cytokines with TAM, the induction characteristics of a number of IFN-induced mRNAs in response to IFNs, TNF, and TAM were studied. We observed an augmentation of the cytotoxic effect of TNF when it was combined with TAM. There appears to be an overlap in signalling mechanisms of IFNs and TNF as two of the IFN-inducible genes, 1-8 and 6-16 are also induced by TNF. mRNA 1-8 was induced by both IFN-alpha (type I) and IFN-gamma (type II). We conclude that TNF potentiates the cytotoxic effects of TAM in MCF-7 cells and that the three cytokines IFN-alpha, IFN-gamma, and TNF share some pathways that lead to specific induction of some cytokine responsive genes.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Rapid induction of nucleoside-diphosphate kinase in HeLa S3 cells by human-type interferons.

Nucleoside-diphosphate (NDP)-kinase can be considered to be induced by human-type interferons (HuIFNs) rapidly, since an enzyme increase was detected within 2 h of incubation of HeLa S3 cells with HuIFNs, while incubation with heterologous mouse IFNs had no such effect. The enzyme increase induced by HuIFNs reached a plateau at 6 h after treatment. Actinomycin D (0.5 microgram/ml) significantly blocked the enzyme increase induced by HuIFNs in the cells. A possible biological role of the enzyme in the IFN-induced biochemical events is discussed.

Adenosine Diphosphate↗
PubMed1991

[Effect of double-stranded RNA and interferon type I on reproduction of cytomegalovirus in human fibroblasts].

Double-stranded RNAs (dsRNA) - larifan and ridostin, and recombinant interferons-alpha-2 and beta-1, manufactured in the USSR, inhibited the reproduction of CMV in cell culture. Antiviral effect depended on concentration of preparations, time of administration and m. o. i. DEAE-dextran enhances antiviral effect dsRNA. DsRNA and interferons added to cells infected with CMV at high m. o. i. enhance the viral reproduction. Among studied preparations highest antiviral effect was shown by natural leucocyte interferon (Egis). It was 10 times more active, than recombinant IFNs and in concentration of 1000 U/ml was comparable to activity of larifan (200 mg/ml).

Antiviral Agents↗
PubMed1987

[Expression of human leukocyte interferon type A in Saccharomyces cerevisiae under the control of regulatory elements of the yeast gene URA3].

Expression of a chromosomal gene for human leucocyte interferon A was obtained due to interaction of 5'-nontranslating region of a cloned interferon gene with the regulatory sequences from UNA3 yeast gene. The sequence of 5'-nontranslating region from interferon gene essential for its expression in yeast is localized within 130 b p. from the initiating codon. Due to increasing of plasmid stability and copy number a 60-fold increase. in interferon yield was obtained in yeast transformants reaching the level of 6 X 10(7) u X 1(-1). The data are presented supposing the existence of functional polycistronic mRNA in yeast.

Base Sequence↗
PubMed1991

[Phosphorylation of proteins in cytoplasmic and nuclear fractions of human cells treated with double-helical RNA and human recombinant interferon type I].

The dynamics of protein kinases activity in nuclear and cytoplasmic fractions of human fibroblasts treated by preparations of natural and synthetic dsRNA (ridostin, rifastin, larifan and poly(I).poly(C), DEAE-dextran and dsRNA complexes with DEAE-dextran), as well as by preparations of recombinant alpha-2 and beta-1 interferons was obtained. The early activation of enzymes in treated cells extracts and their presence in dsRNA-activated and nonactivated forms were found. In cytoplasmic cellular fractions treated by interferons the dsRNA dependent protein kinases (nonactivated forms- were prevalent.r In contrast, in dsRNA treated cells or dsRNA complexes with DEAE-dextran treated ones the dsRNA independent protein kinases (activated forms) were found, while dsRNA dependent forms induced by interferons were found at later periods. Nuclear protein kinases are mainly dsRNA independent making possible the supposition of their intracellular activation by incoming dsRNA or interferon-induced formation of ds-structures in cellular nuclei. In phosphorylated proteins spectre the 90, 69, 45-40 and 30-35 kDa polypeptides were found. At early intervals in nuclear fractions was found a nuclease resistant and partially EDTA resistant high molecular phosphorylated complex (120 kDa). The complex is, probably, capable of dissociation to low mol mass components. DEAE-dextran induces strong activation of protein kinases in cytoplasm and nuclei and increases the content of activated forms of enzyme in larifan treated cells.

Cell Nucleus↗
PubMed1985

In vitro production of different interferon types by cloned human NK cells.

Human peripheral blood null cells were conjugated in vitro with K-562 cells and expanded into continuous cell lines using IL-2 containing medium (CM) and periodical restimulation with phytohaemagglutinin (PHA). Most of these lines were made up of granular blasts expressing high natural killer (NK) activity. When analysed for different surface markers, the large majority of the blasts were E rosette+, T3+, Tac+, DR+, Leu7+ with a variable proportion of cells expressing T8 and M1 antigens (range: 20-80%). In contrast, T4 antigen was expressed by the majority of cells of the control cell lines originated in the absence of K-562 cells. Twenty-nine clones were obtained from one of the above lines using the limiting dilution technique and subsequently maintained in CM for 4 months or more. The majority of these clones maintained their cytotoxic potential and were able to produce different interferon (IFN) types (IFN-alpha, IFN-gamma or both) when growing in CM. In addition in a number of selected clones, simultaneous stimulation with PHA and K-562 cells was able to induce or support the production of both IFN types.

Antigens, Surface↗
PubMed1987

Immunoferon (AM3) enhances the activities of early-type interferon inducers and natural killer cells.

The "in vivo" effect of Immunoferon (AM3) on the production of interferon (IFN) and natural killer (NK) activity in young and old mice was studied. Although AM3 is not an IFN inducer by itself, enhancements in the serum IFN levels were produced when drug was associated to Newcastle disease virus or bacterial lipopolysaccharides as IFN inducers. This effect appeared to be dependent on the time lapsed between the inducer agent and drug. In addition, a significant stimulating effect on NK cell activity was also produced by AM3 treatments. This effect could be a consequence of a marked IFN induction and/or a modifying effect in prostaglandin synthesis.

Animals↗
PubMedDate not supplied

[Monoclonal antibodies to natural human gamma-type interferon].

Nine hybridomas producing monoclonal antibodies (MCA) to natural human gamma interferon (IF-gamma) were generated. BALB/c mice were immunized with nonpurified IF-gamma preparation synthesized by lymphoid cells of the peripheral blood of donors in response to induction with staphylococcal enterotoxin A. For the first time somatic hybridization was done with the use of a medium with a high content of HEPES which maintained hybridomas viable for a long period of time. Out of 9 hybridomas, two (-gamma 6.1 and gamma-8.1) were shown to produce MCA with a high binding activity in the enzyme immunoassay. The same MCA effectively neutralized the biological activity of natural IF-gamma.

Animals↗
PubMed1986

Modulation of lymphocyte proliferation and immunoglobulin synthesis by interferon-gamma and "type I" interferons.

Interferon (IFN)-alpha and IFN-beta ("type I" IFNs), but not IFN-gamma reduced phytohemagglutinin- or pokeweed mitogen (PWM)-induced proliferation in cultures of human mononuclear leukocytes. Proliferation induced by specific antigens (tuberculin PPD or tetanus toxoid) or by exogenous interleukin 2 (IL-2) was strongly inhibited by type I IFNs and, to a lesser extent, by IFN-gamma as well. Inhibition of proliferation in mitogen-stimulated cultures was not due to a reduced production of IL-2 or to an inhibition of IL-2 receptor expression. Type I IFNs inhibited immunoglobulin (Ig) production in PWM-stimulated unseparated mononuclear cells, whereas IFN-gamma enhanced Ig production in such cultures. In cultures of purified B cells type I IFNs caused a stimulation of Ig production and this B-cell differentiation factor (BCDF)-like activity of IFNs was synergistically enhanced in the presence of IL-2. IFN-gamma produced less BCDF-like activity than type I IFNs. These results show that in some instances type I IFNs can be more potent in affecting functions of cells of the immune system than IFN-gamma.

Antibody Formation↗
PubMedDate not supplied

Effects of phenytoin on the production of interferons: differential effects on type I and type II interferons.

The relative effects of treatment with an anticonvulsant, phenytoin, on the production of interferons were determined for both the murine and human systems. Phenytoin treatment was found to have differential effects on the in vitro production of Type I and Type II interferons. Phenytoin had either no effect (HuIFN-alpha) or an enhancing effect (MuIFN-alpha/beta) on the in vitro production of Type I interferons. In contrast, phenytoin pretreatment had an inhibitory effect on the in vitro production of Type II interferons (IFN-gamma) for both the murine and human systems. Phenytoin appeared to exert its inhibitory effect directly on the IFN-gamma-producing cell and was active even when added as late as 6 h after IFN-gamma induction. This inhibition was not related to a toxic effect of the phenytoin and occurred at phenytoin concentrations which were pharmacologically relevant (10-20 micrograms/ml). The effects of phenytoin on the in vivo production of MuIFN-gamma were also examined. In parallel to the in vitro observations, phenytoin treatment of mice significantly reduced the in vivo induction of MuIFN-gamma. The results raise the possibility that phenytoin therapy in humans may significantly affect the production of HuIFN-gamma.

Animals↗
PubMed1979

Immune-type interferon-induced transfer of viral resistance.

Mouse immune-type interferon (type II), a lymphokine, caused the transfer of viral resistance from mouse L cells to human WISH cells. The interferon was incapable of protecting WISH cells in the absence of L cells. The transfer of viral resistance occurred with interferon preparations of various specific activities, and was in proportion to the interferon concentration in the preparations. The transferred resistance had the characteristics of an interferon-induced antiviral state in that it was blocked by actinomycin D, effective against different types of viruses, and resulted from an action on the cell rather than on the virus. Mouse immune-type interferon was more efficient than virus-type (type I) at eliciting the transfer of protection. The transfer phenomenon may represent a mechanism for amplification of the interferon system as a host defense against viral infection. Further, it serves as a model for studying the mechanism of lymphokine-induced transfer of information between cells.

Animals↗
PubMed1979

In vitro production and cellular origin of murine type II interferon.

Antigen-specific type II interferon was produced in vitro by harvesting supernatants of spleen cell cultures from Swiss-Webster mice sensitized with Mycobacterium bovis strain BCG and challenged with old tuberculin. Treatment of C3H mouse spleen cell cultures with appropriate anti-Ia, anti-IgG, anti-Thy-1 or anti-Ly-2,3 sera resulted in a significant decrease in production of type II interferon. Removal of nylon wool adherent cells or cells with histamine receptors by column chromatography similarly caused reduced production of type II interferon. Recombination of spleen cell cultures treated with anti-Ia and anti-Thy-1 sera or of cells treated with anti-IgG and anti-Thy-1 resulted in restored production of type II interferon. Interferon production was also restored by combination of cells passed through histamine columns with anti-Ia treated cells, or those passed through nylon wool columns with anti-Thy-1 treated cells. Anti-Ly-1 serum treatment had no effect on interferon production. Removal of plastic-adherent cells or cells that had phagocytosed carbonyl iron also decreased interferon production, suggesting that macrophages were also involved in type II interferon production. Recombination of non-adherent spleen cells with anti-Ia and anti-Thy-1 sera treated spleen cells, however, did not restore interferon production, suggesting that other cells in addition to macrophages are depleted by the adherence procedure. These findings indicate that type II interferon is produced by suppressor or cytotoxic (Ly-2,3+) T lymphocytes in co-operation with one or two additional cell types: (i) B lymphocytes, and (ii) macrophages.

Animals↗