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Ability of the Matrix Protein of Vesicular Stomatitis Virus To Suppress Beta Interferon Gene Expression Is Genetically Correlated with the Inhibition of Host RNA and Protein Synthesis

Ahmed, Maryam; McKenzie, Margie O.; Puckett, Shelby; Hojnacki, Michael; Poliquin, Laurent; Lyles, Douglas S.
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /04/2003 Português
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The vesicular stomatitis virus (VSV) matrix (M) protein plays a major role in the virus-induced inhibition of host gene expression. It has been proposed that the inhibition of host gene expression by M protein is responsible for suppressing activation of host interferon gene expression. Most wild-type (wt) strains of VSV induce little if any interferon gene expression. Interferon-inducing mutants of VSV have been isolated previously, many of which contain mutations in their M proteins. However, it was not known whether these M protein mutations were responsible for the interferon-inducing phenotype of these viruses. Alternatively, mutations in other genes besides the M gene may enhance the ability of VSV to induce interferons. These hypotheses were tested by transfecting cells with mRNA expressing wt and mutant M proteins in the absence of other viral components and determining their ability to inhibit interferon gene expression. The M protein mutations were the M51R mutation originally found in the tsO82 and T1026R1 mutant viruses, the double substitution V221F and S226R found in the TP3 mutant virus, and the triple substitution E213A, V221F, and S226R found in the TP2 mutant virus. wt M proteins suppressed expression of luciferase from the simian virus 40 promoter and from the beta interferon (IFN-β) promoter...

Different mRNAs induced by interferon in cells from inbred mouse strains A/J and A2G.

Staeheli, P; Colonno, R J; Cheng, Y S
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1983 Português
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Treatment of cells from inbred mouse strains A/J and A2G with interferon resulted in the development of different antiviral states for influenza viruses. A2G mice-derived cells that carry the resistance gene Mx were efficiently protected by interferon against influenza viruses, whereas the interferon protection against the same viruses in wild-type A/J mice-derived cells was only marginal. The two cell types, however, were equally protected by interferon against vesicular stomatitis virus and other non-orthomyxoviruses. The interferon-induced mRNAs of mouse embryonic fibroblast cells that carried either homozygous wild-type alleles or homozygous Mx alleles were compared. The isolated polysome-bound mRNAs from A/J (+/+) and A2G (Mx/Mx) cells were translated in a cell-free translation system, and the translation products were analyzed after two-dimensional gel electrophoresis. New mRNAs coding for at least eight proteins with molecular weights (MW) ranging from 30,000 to 80,000 were found in interferon-treated cells but not in control cells. Differences in the interferon-induced mRNAs from A/J and A2G cells were also found. An mRNA coding for a 72,000-MW protein was found in interferon-treated A2G cells but not in interferon-treated A/J cells. Interferon-treated A/J cells...

Production of gamma interferon in mice immune to Rickettsia tsutsugamushi.

Palmer, B A; Hetrick, F M; Jerrells, T J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /01/1984 Português
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C3H/He mice immunized by subcutaneous infection with Rickettsia tsutsugamushi Gilliam were examined for the production of immune interferon after intravenous administration of irradiated strain Gilliam antigen, in supernatants of immune lymphocytes stimulated with specific antigen, and after a secondary challenge with viable rickettsiae. Mice administered various doses of irradiated whole-organism antigen 28 days after immunization showed circulating levels of interferon which peaked 4 h after inoculation and were antigen dose dependent. The interferon produced was pH 2 sensitive and stable at 56 degrees C for 1 h and was neutralized by antiserum directed against immune, but not against alpha/beta, interferon. The production of another lymphokine, macrophage migration inhibition factor, paralleled that of interferon. The interferon produced by cultures of spleen cells obtained from immune animals was antigen specific and dose dependent. Peak levels were obtained 48 to 72 h after the addition of antigen. The interferon produced by spleen cell cultures after stimulation with Gilliam antigen was characterized as immune interferon by the same physical and antigenic criteria used for serum interferon. Interferon was produced in vitro by the Thy-1.2+ lymphocyte and required the presence of a spleen-adherent cell population. Immune mice produced high circulating levels of immune interferon after intraperitoneal challenge with viable rickettsiae...

PRODUCTION OF AN INTERFERON BY L CELLS INFECTED WITH WESTERN EQUINE ENCEPHALOMYELITIS VIRUS

Lockart, Royce Z.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1963 Português
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Lockart, Royce Z., Jr. (The University of Texas, Austin). Production of an interferon by L cells infected with Western equine encephalomyelitis virus. J. Bacteriol. 85:556–566. 1963.—Two strains of Western equine encephalomyelitis virus (WEE), WEE (L+) and WEE (L−), which differed with respect to their cytopathogenicity for L cells were isolated. Both strains reproduced in L cells, and both induced the production of an interferon distinct from virus particles. L-cell monolayers were protected from degeneration by prior addition of interferon. By use of the absence of cytopathic effects (CPE) as an end point, interferon content was assayed. Monolayers failing to show CPE consistently produced less than 2% as much virus as control monolayers, indicating that virus synthesis was also inhibited. The use of this assay method was facilitated by the use of horse serum that appeared to contain antibodies against WEE and that permitted interferon to act selectively in the presence of active virus. It was found that interferon was produced during the time in which active virus was produced, and not significantly later. No interferon could be found in fluids from cells treated with inactive virus, although these are known to act as interfering agents. Interferon production was inhibited by pretreatment of L cells with sufficient amounts of interferon. It is concluded that interferon production is closely connected with WEE virus synthesis in L cells. The question is raised as to whether interferon need be a necessary intermediate for interference in L cells.

Recombinant interferon-gamma primes alveolar macrophages cultured in vitro for the release of leukotriene B4 in response to IgG stimulation.

Rankin, J A; Schrader, C E; Smith, S M; Lewis, R A
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /05/1989 Português
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The capacity of interferon-gamma to regulate the generation and release of leukotriene B4 (LTB4) from human alveolar macrophages of normal nonsmoking individuals was evaluated. When alveolar macrophages were incubated for 60 min with heat aggregated IgG (HAIgG), they generated and released 5.7 +/- 1.7 ng of LT B4 per 10(6) cells compared to 1.9 +/- 0.4 ng from cells incubated with buffer alone, P = 0.02. When alveolar macrophages were preincubated with interferon-gamma for 24 h before activation for 60 min with heat-aggregated IgG, the soluble IgG aggregates became a significantly more effective stimulus for LTB4 release, 17.0 +/- 3.9 ng/10(6) cells, P = 0.001, compared to cells incubated in the absence of interferon-gamma and challenged with HAIgG. Interferon-gamma did not alter the response to A23187. This effect of interferon-gamma was both time and dose dependent; it also was specific since neither interferon-alpha nor interferon-beta had a regulatory effect on the release of LTB4 from cells in response to challenge with HAIgG. Preincubation of the alveolar macrophages with interferon-gamma augmented the density of IgG1 receptors by 81.5 +/- 17.3%; neither interferon-alpha nor interferon-beta effected this parameter. Furthermore...

Natural Cytotoxicity to Murine Cytomegalovirus-Infected Cells Mediated by Mouse Lymphoid Cells: Role of Interferon in the Endogenous Natural Cytotoxicity Reaction

Lee, Gerald D.; Keller, Robert
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /01/1982 Português
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Lymphoid cells from unstimulated normal C57BL/6J mice were shown to lyse murine cytomegalovirus (MCMV)-infected syngeneic mouse embryo fibroblasts but not uninfected mouse embryo fibroblasts. This cytotoxicity by mouse effector cells was not restricted to MCMV-infected syngeneic cells since MCMV-infected xenogeneic rat heart fibroblasts were also lysed. Characterization of the effector cells mediating this cytotoxicity against MCMV-infected cells indicated that the effector cells are similar to described natural killer (NK) cells mediating lysis of tumor cells and virus-infected cells. Because of the described augmentation of NK activity by interferon, we examined the role of interferon in the NK reaction. Although low levels of virus-induced interferon were detectable in supernatants of MCMV-infected mouse embryo fibroblasts, no interferon was detectable in supernatants of MCMV-infected rat heart fibroblasts, a target significantly more sensitive to NK cytolysis than infected mouse embryo fibroblasts. We were able to augment the NK reaction against MCMV-infected cells by in vitro treatments with interferon. However, the amounts of interferon required for augmentation were significantly greater than the amounts generated by infected target cells. In vitro interferon-stimulated NK cells retained selective cytotoxic activity since they continued to remain incapable of lysing uninfected target cells. MCMV-infected rat heart fibroblasts induced more interferon and were also more susceptible to NK activity than MCMV-infected mouse embryo fibroblasts. In spite of this difference in interferon-inducing capacity...

Mechanism of immune interferon production in vitro: interaction between immune interferon-producing cells and antigenic cells.

Ito, Y; Aoki, H; Kimura, Y; Shimokata, K; Maeno, K
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1981 Português
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Various processes of in vitro immune interferon production by sensitized spleen cells stimulated with allogeneic cells were investigated. When L cells, an interferon-inducing antigen, were fixed with methyl alcohol or paraformaldehyde, the ability to induce immune interferon disappeared. In this immune interferon production system, the majority of sensitized spleen cells adhered to target cells within 1 h of cocultivation. Adherence of immune interferon-producing cells to target cells was observed only when L cell-sensitized spleen cells were cocultured with L cells or with mouse embryo cells derived from C3H mice. Fixation of antigenic cells with methyl alcohol or paraformaldehyde significantly reduced cell adherence. When L cells alone or sensitized spleen cells alone were pretreated separately with cytochalasin D, neither cell type could bind to partner cells. Specific adherence did not take place at 4 degrees C, nor in the presence of dinitrophenol or sodium azide. Continuous protein synthesis in both cells was not required for immune cell adherence. Divalent cations, Ca2+ or Mg2+, were required for this immune specific adherence to take place. However, once stable adherence was established, treatment with cytochalasin D, ethylenediaminetetraacetic acid...

Recovery of Cell-Bound Interferon

Stewart, William E.; De Clercq, Erik; De Somer, Pierre
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /10/1972 Português
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Interferon could be recovered from homologous cells to which it was applied but could not be recovered from heterologous cells. The amount of interferon that could be recovered from cells corresponded to the sensitivity of the cells to the antiviral activity of the interferon: mouse embryo fibroblasts, which were 5 to 10 times as sensitive as L-929 cells to interferon, bound 5 to 10 times more interferon than the latter, whereas Lpa cells, which were only one-third as sensitive as L-929 cells to interferon, bound only one-third as much as the latter. The concentration of cell-bound interferon was as much as 150 times the extracellular concentration of interferon applied to the cells. Interferon bound to cells at 4 C with the same efficiency as it did to cells at 37 C, and actinomycin D-treated cells bound interferon as well as normal cells. Even though the total amount of interferon bound to cells was as much as 30% of the amount of interferon applied to them, no loss of antiviral activity was detectable from the medium.

Interferon-Inducing Characteristics of MM Virus

Giron, D. J.; Allen, P. T.; Pindak, F. F.; Schmidt, J. P.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1971 Português
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Interferon induction by MM virus in mice and in L cells was studied. In mice the virus readily induced interferon. The time of appearance was dose-dependent. A large virus dose induced interferon by 4 hr, whereas a small dose resulted in interferon production which paralleled virus replication 24 hr after infection. In L cells the interferon-inducing capacity of the virus was rapidly destroyed by ultraviolet light irradiation. Heating (56 C) of the virus, on the other hand, greatly increased its ability to induce interferon. Interferon production could also be increased by prior treatment of the cells with homologous interferon (priming). The increase in interferon production after priming was dependent on the concentration of interferon used for priming, the length of interferon treatment, and the multiplicity of infection. It is suggested that MM virus might be useful for the further study of the mechanisms involved in the production and action of interferon.

Rapid and transient rise in diacylglycerol concentration in Daudi cells exposed to interferon.

Yap, W H; Teo, T S; McCoy, E; Tan, Y H
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /10/1986 Português
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Human beta-interferon stimulates a 4-fold increase in the concentration of diacyglycerol and a 2-fold increase in the concentration of inositol monophosphate in Daudi (human B-lymphoblastoid) cells within 30 sec of exposure of the cells to interferon. The increase in diacylglycerol and in inositol monophosphate is transient and the concentrations of these compounds decrease to basal levels within 10 min. Preincubation of human beta-interferon with anti-interferon antibodies inhibits this effect as well as the binding of interferon to Daudi cells. Diacylglycerol concentrations were unaffected in mouse A9 cells (fibroblasts) incubated with human beta-interferon and in Daudi cells incubated with human gamma-interferon. Mouse A9 cells are insensitive to human interferon and Daudi cells are insensitive to human gamma-interferon. The magnitude of the increase in diacylglycerol concentration stimulated by interferon can be correlated to the interferon-induced inhibition of Daudi cell division in a dose-responsive manner. Phorbol 12-myristate 13-acetate also inhibits Daudi cell division in a dose-responsive manner. It is likely that the sharp and transient increase in diacylglycerol concentration represents one of the early biochemical changes in Daudi cells exposed to interferon.

Large-scale production and physicochemical characterization of human immune interferon.

Langford, M P; Georgiades, J A; Stanton, G J; Dianzani, F; Johnson, H M
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /10/1979 Português
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Large-scale production of crude high-titered (10(2.3) to 10(4) U/ml) human immune interferon (type II) was carried out in roller bottle cultures of human peripheral lymphocytes by using the T-cell mitogen staphylococcal enterotoxin A. Over 99% of human immune interferon was destroyed by pH 2 or heat at 56 degrees C for 1 h. The interferon was not neutralized by antibody to human leukocyte interferon. The kinetics of development of the antiviral state were slow for immune interferon relative to those for leukocyte interferon. Ultrogel AcA 54 chromatography of crude or the concentrated interferon resulted in two peaks of activity, a major one (87% of recovered activity) with a molecular weight of 40,000 to 46,000 and a minor peak of molecular weight 65,000 to 70,000. The column elution buffer consisting of 18% ethylene glycol and 1 M NaCl in phosphate-buffered saline resulted in at least 100% recovery of added interferon. The data suggest, then, that the interferon produced under large-scale conditions was immune (type II). The efficiency of the production was comparable to that described for large-scale production of human leukocyte interferon. Our large-scale production system for human immune interferon offers a feasible approach to preparation of large quantities of purified immune interferon for structure studies...

Role of IL-2 and interferon in the generation of natural cytotoxic activity in influenza virus-stimulated PBL cultures: analysis with the use of prednisolone.

Braakman, E; Treep-van Leeuwen, P; ten Berge, R J; Schellekens, P T; Lucas, C J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /02/1988 Português
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We have examined the role of interleukin 2, interferon-gamma and interferon-alpha in the generation of natural cytotoxic (NC) activity and cytotoxic T-lymphocyte (CTL) activity in peripheral blood lymphocyte cultures stimulated with influenza virus, using the immunosuppressive effects of prednisolone. In addition to an inhibitory effect on the generation of CTL activity, prednisolone also inhibited the generation of NC activity in a similar dose-and time-dependent manner. Prednisolone suppressed the production of interferon-gamma when it was added on the first day of culture of PBL with influenza virus. Levels of interferon-alpha were not affected. The effects of prednisolone on the generation of NC activity and CTL activity in kinetic terms were not paralleled by the effects on interferon-alpha and interferon-gamma production. The diminished generation of NC activity could be reversed by the addition of interleukin 2 (IL-2), but interferon-gamma had little if any restorative effects. Interferon-alpha had no effect. These findings support the hypothesis that IL-2 is the major inducer of NC activity in CTL generation cultures. The inhibitory effect on CTL generation could only be reversed by IL-2 and not by interferon-alpha- and interferon-gamma. Thus...

Cloned mouse interferon-gamma inhibits the growth of Rickettsia prowazekii in cultured mouse fibroblasts

Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/12/1983 Português
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The effect of treating cultured mouse fibroblasts (L929 cells) with cloned mouse interferon-gamma on the growth of Rickettsia prowazekii within the fibroblasts was studied. Within 48 h after infection, rickettsiae were cleared from a substantial proportion of the initially infected cells and rickettsial growth was inhibited in those cells that remained infected, when L929 cells were treated with cloned mouse interferon-gamma both before and after infection. When L929 cells were treated with cloned mouse interferon-gamma either only before or only after infection with rickettsiae, rickettsial growth was markedly inhibited but rickettsiae were not cleared from many cells. Addition of cycloheximide to L929 cells markedly suppressed the antirickettsial activity of the interferon, and cloned mouse interferon-gamma did not induce antirickettsial activity in human foreskin fibroblasts. The antirickettsial effects of cloned mouse interferon-gamma were similar to those induced by crude mouse lymphokines prepared from concanavalin A-stimulated mouse spleen cells. Equivalent amounts (units) of cloned mouse interferon-gamma produced by Chinese hamster ovary cells or by Escherichia coli caused equivalent inhibition of rickettsial growth in mouse fibroblasts. However...

The Alpha/Beta Interferon Receptor Provides Protection against Influenza Virus Replication but Is Dispensable for Inflammatory Response Signaling ▿ †

Goodman, Alan G.; Zeng, Hui; Proll, Sean C.; Peng, Xinxia; Cillóniz, Cristian; Carter, Victoria S.; Korth, Marcus J.; Tumpey, Terrence M.; Katze, Michael G.
Fonte: American Society for Microbiology (ASM) Publicador: American Society for Microbiology (ASM)
Tipo: Artigo de Revista Científica
Português
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The innate immune response provides the first line of defense against foreign pathogens by responding to molecules that are a signature of a pathogenic infection. Certain RNA viruses, such as influenza virus, produce double-stranded RNA as an intermediate during the replication life cycle, which activates pathogen recognition receptors capable of inducing interferon production. By engaging interferon receptors, interferon activates the JAK-STAT pathway and results in the positive feedback of interferon production, amplifying the response to viral infection. To examine how deficiencies in interferon signaling affect the cellular response to infection, we performed influenza virus infections of mouse embryonic fibroblasts lacking the alpha/beta interferon receptor, the gamma interferon receptor, or both. In the absence of the alpha/beta interferon receptor, we observed increased viral replication but decreased activation of PKR, Stat1, and NF-κB; the presence or absence of the gamma interferon receptor did not exhibit discernible differences in these readouts. Analysis of gene expression profiles showed that while cells lacking the alpha/beta interferon receptor exhibited decreased levels of transcription of antiviral genes, genes related to inflammatory and apoptotic responses were transcribed to levels similar to those of cells containing the receptor. These results indicate that while the alpha/beta interferon receptor is needed to curb viral replication...

SIMIAN IMMUNODEFICIENCY VIRUS INFECTION IN THE BRAIN AND LUNG LEADS TO DIFFERENTIAL TYPE I INTERFERON SIGNALING DURING ACUTE INFECTION*

Alammar, Luna; Gama, Lucio; Clements, Janice E.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Português
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Using an accelerated and consistent simian immunodeficiency virus (SIV) pigtailed macaque model of HIV associated neurological disorders, we have demonstrated that virus enters the brain during acute infection. However, neurological symptoms do not manifest until late stages of infection, suggesting that immunological mechanisms exist within the central nervous system (CNS) that control viral replication and associated inflammation. We have shown that interferon beta, a type I interferon central to viral innate immunity, is a major cytokine present in the brain during acute infection and is responsible for limiting virus infection and inflammatory cytokine expression. However, the induction and role of interferon alpha in the CNS during acute SIV infection has never been examined in this model. In the classical model of interferon signaling, interferon beta signals through the interferon α/β receptor, leading to expression of interferon alpha. Surprisingly, although interferon beta is up regulated during acute SIV infection, we found that interferon alpha is down regulated. We demonstrate that this down regulation is coupled with a suppression of signaling molecules downstream of the interferon receptor, namely tyk2, STAT1 and IRF7...

Delayed Cytosolic Exposure of Japanese Encephalitis Virus Double-Stranded RNA Impedes Interferon Activation and Enhances Viral Dissemination in Porcine Cells▿†

Espada-Murao, Lyre Anni; Morita, Kouichi
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /07/2011 Português
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Interferon is a principal component of the host antiviral defense system. In this study, abortive focus formation by Japanese encephalitis virus (JEV) in primate cells was accompanied by early interferon induction, while productive focus formation in porcine cells was associated with a late interferon response. Neutralization antibodies against interferon relieved the restricted infection in primate cells, and increasingly larger foci were generated as treatment with exogenous interferon was delayed, thereby establishing a solid correlation between interferon response and viral dissemination. However, delayed interferon induction in JEV-infected porcine cells occurred in the absence of active inhibition by the virus. We further demonstrated that JEV mediates interferon activation through double-stranded RNA and cytosolic pattern recognition receptors. Immunofluorescence and subcellular fractionation studies revealed that double-stranded RNA is concealed in intracellular membranes at an early phase of infection but eventually appears in the cytosol at later periods, which could then allow detection by cytosolic pattern recognition receptors. Interestingly, cytosolic exposure of double-stranded RNA was delayed in porcine cells compared to primate cells...

Multiple Sclerosis: Modulation of Toll-Like Receptor (TLR) Expression by Interferon-β Includes Upregulation of TLR7 in Plasmacytoid Dendritic Cells

Derkow, Katja; Bauer, Jakob M. J.; Hecker, Michael; Paap, Brigitte K.; Thamilarasan, Madhan; Koczan, Dirk; Schott, Eckart; Deuschle, Katrin; Bellmann-Strobl, Judith; Paul, Friedemann; Zettl, Uwe K.; Ruprecht, Klemens; Lehnardt, Seija
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 12/08/2013 Português
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Interferon-β is an established treatment for patients with multiple sclerosis (MS) but its mechanisms of action are not well understood. Viral infections are a known trigger of MS relapses. Toll-like receptors (TLRs) are key components of the innate immune system, which sense conserved structures of viruses and other pathogens. Effects of interferon-β on mRNA levels of all known human TLRs (TLR1-10) and the TLR adaptor molecule MyD88 were analyzed in peripheral blood mononuclear cells (PBMCs) of healthy donors by quantitative real-time PCR and by transcriptome analysis in PBMCs of 25 interferon-β-treated patients with relapsing-remitting MS. Regulation of TLR protein expression by interferon-β was investigated by flow cytometry of leukocyte subsets of healthy subjects and of untreated, interferon-β-, or glatiramer acetate-treated patients with MS. Interferon-β specifically upregulated mRNA expression of TLR3, TLR7, and MyD88 and downregulated TLR9 mRNA in PBMCs of healthy donors as well as in PBMCs of patients with MS. Plasmacytoid dendritic cells (pDCs) were identified as the major cell type responding to interferon-β with increased expression of TLR7 and MyD88 protein. In line with this, expression of TLR7 protein was increased in pDCs of interferon-β-treated...

Induction of human beta-interferon synthesis with poly(rI . rC) in mouse cells transfected with cloned cDNA plasmids.

Pitha, P M; Ciufo, D M; Kellum, M; Raj, N B; Reyes, G R; Hayward, G S
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /07/1982 Português
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Human genomic DNA and plasmids carrying portions of the cDNA gene for human beta-interferon have been introduced into mouse Ltk- cells by cotransfection with a herpes simplex virus thymidine kinase (TK) gene. One plasmid contains 840 base pairs of human DNA complementary to pre-beta-interferon mRNA inserted into pBR322, whereas the other plasmids have hybrid genes containing only the 560-base pair coding region inserted under the transcriptional control of the TK promoter. Constitutive interferon production could not be detected in any of the mouse TK+ cell lines tested. Nevertheless, synthesis of interferon could be induced by poly(rI . rC) treatment in at least 16 of these cell lines, including clones transfected with genomic DNA, the beta-interferon cDNA, and the TK-beta-interferon cDNA hybrid gene. The interferon produced was specific for human cells and could be neutralized by antiserum against human beta-interferon. In contrast to human fibroblast cells, in which the synthesis of induced beta-interferon is transient, the poly(rI . rC)-induced TK+ lines continued to produce beta-interferon for prolonged periods of time and did not respond to superinduction conditions. Therefore, in transfected mouse cells, the coding DNA sequence from the human beta-interferon gene...

Regulation of the stability of poly(I)xpoly(C)-induced human fibroblast interferon mRNA: selective inactivation of interferon mRNA and lack of involvement of 2',5'-oligo(A) synthetase activation during the shutoff of interferon production.

Sehgal, P B; Gupta, S L
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1980 Português
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The inactivation of interferon mRNA during the shutoff phase of interferon production in poly(I)xpoly(C)-induced human fibroblast cultures is selective. We have determined that the shutoff of interferon production, which takes place from 3 to 8 hr after the beginning of induction, is not associated with an appreciable declined in the rate of bulk cellular protein synthesis or of cellular protein secretion. While the amount of translatable interferon mRNA declined markedly during the shutoff phase, the level of translatable bulk cellular mRNA and the stability of [3H]uridine-labeled mRNA were unaffected. Superinduction with actinomycin D selectively stabilized interferon mRNA with no apparent effect on the stability of bulk cellular mRNA. Furthermore, an activation of the 2',5'-oligo(A) synthetase/endonuclease system does not appear to be involved in the shutoff phenomenon. Uninduced FS-4 cells contained a low basal level of 2'5'-oligo(A) synthetase activity, which was unchanged in poly(I)xpoly(C)-induced cells during the shutoff phase. Treatment of FS-4 cells with interferon for 16-18 hr prior to induction increased the enzyme activity by approximately 200-fold. However, this did not inhibit interferon production after induction with poly(I)xpoly(C) alone or after superinduction with cycloheximide or actinomycin D or both. Furthermore...

Interferon modulation of c-myc expression in cloned Daudi cells: relationship to the phenotype of interferon resistance.

Dron, M; Modjtahedi, N; Brison, O; Tovey, M G
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /05/1986 Português
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Treatment of interferon-sensitive Daudi cell with electrophoretically pure human interferon alpha markedly reduced the level of c-myc mRNA, increased the level of class I histocompatibility antigen (HLA) mRNA, and did not affect the level of actin mRNA within the same cells. In contrast, the level of c-myc mRNA or HLA mRNA did not change significantly following interferon treatment in different clones of Daudi cells selected for resistance to the antiproliferative action of interferon. These cells possessed interferon receptors, however, and responded to interferon modulation of other genes, including 2',5' oligoisoadenylate synthetase (M. G. Tovey, M. Dron, K. E. Mogensen, B. Lebleu, N. Metchi, and J. Begon-Lours, Guymarho, J. Gen. Virol., 64:2649-2653, 1983; M. Dron, M. G. Tovey, and P. Eid, J. Gen. Virol., 66:787-795, 1985). A clone of interferon-resistant Daudi cells which had reverted to almost complete sensitivity to both the antiproliferative action of interferon and the interferon-enhanced expression of HLA mRNA remained refractory, however, to interferon modulation of c-myc expression, suggesting that a reduced level of c-myc mRNA may not be a prerequisite for inhibition of cell proliferation in interferon-treated cells. Our results do not exclude the possibility...