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At least 703 records · Page 39Linked to original sources
PubMed2006

Intrahepatic mRNA levels of type I interferon receptor and interferon-stimulated genes in genotype 1b chronic hepatitis C. Association between IFNAR1 mRNA level and sustained response to interferon therapy.

OBJECTIVE: The aim of this study was to determine the association between pretreatment intrahepatic mRNA levels of interferon receptor and interferon-stimulated genes and response to interferon therapy for genotype 1b chronic hepatitis C. METHODS: Forty-four patients with genotype 1b chronic hepatitis C who underwent liver biopsy and then received interferon therapy participated in this study. Pretreatment intrahepatic mRNA levels of interferon receptor genes (IFNAR1, IFNAR2b, and IFNAR2c) and interferon-stimulated genes (OAS1 and PKR) were quantified by competitive polymerase chain reaction. RESULTS: In the genes examined, only IFNAR1 mRNA level was significantly higher in patients with sustained virological and biochemical response to interferon therapy versus those with nonsustained response (p < 0.01). Moreover, mRNA expression ratios of IFNAR1 to IFNAR2 were also significantly higher in patients with sustained virological and biochemical response to IFN therapy (p < 0.01 and p < 0.05, respectively). On the other hand, mRNA levels of IFNAR2b, IFNAR2c, and PKR were significantly higher in patients with histologically active or advanced liver rather than patients with mild or less advanced liver. CONCLUSIONS: High intrahepatic mRNA levels of IFNAR1 and mRNA ratio of IFNAR1 to IFNAR2 before treatment may be associated with a favorable response to interferon therapy.

2',5'-Oligoadenylate Synthetase↗
PubMed2005

U1 small nuclear ribonucleoprotein immune complexes induce type I interferon in plasmacytoid dendritic cells through TLR7.

Plasmacytoid dendritic cells (PDCs), which produce IFN-alpha in response to autoimmune complexes containing nuclear antigens, are thought to be critically involved in the pathogenesis of systemic lupus erythematosus (SLE). One of the immunostimulatory components of SLE immune complexes (SLE-ICs) is self DNA, which is recognized through Tlr9 in PDCs and B cells. Small nuclear ribonucleoproteins (snRNPs) are another major component of SLE-ICs in 30% to 40% of patients. In this study, we show that murine PDCs are activated by purified U1snRNP/anti-Sm ICs to produce IFN-alpha and proinflammatory cytokines and to up-regulate costimulatory molecules. The induction of IFN-alpha and IL-6 by U1snRNPs in murine bone marrow-derived PDCs required the presence of intact U1RNA and was largely dependent on Tlr7 but independent of Tlr3. Intracellularly delivered isolated U1snRNA and oligoribonucleotides derived from the stem loop regions and the Sm-binding site of U1snRNA efficiently induced IFN-alpha and IL-6 in Flt3L-cultured DCs in a Tlr7-dependent manner. The U1snRNA component of U1snRNP immune complexes, found in patients with SLE, acts as an endogenous "self" ligand for Tlr7 and triggers IFN-alpha and IL-6 production in PDCs.

Animals↗
PubMed2000

Type I interferon production in cattle infected with 2 strains of foot-and-mouth disease virus, as determined by in situ hybridization.

Four calves were exposed via aerosol to 1 of 2 strains of foot-and-mouth disease virus. Two animals received virus derived from an infectious clone virus (A12-IC) and 2 received virus derived from the same clone but which lacked the leader coding region (A12-LLV2) that codes for a protein responsible for turning off host protein synthesis. Animals were euthanized at 24 and 72 h post exposure. Cattle receiving A12-IC had a rapid course of disease with more virus in tissues while A12-LLV2-infected cattle did not develop clinical signs of disease. Formalin-fixed, paraffin-embedded tissue sections were probed with digoxigenin-labeled riboprobes corresponding to the coding sequence for bovine interferon (IFN) alpha and IFNbeta. Staining for IFNalpha mRNA was noted in mononuclear cells of the lungs of all animals and in respiratory lymph nodes of cattle receiving A12-IC. Staining for IFNbeta mRNA was confined to bronchiolar epithelium and present only in the animals infected with A12-IC. Inability of the A12-LLV2 virus to achieve levels of spread seen with A12-IC may be related to translation of IFNalpha in A12-LLV2-infected cells, which renders adjacent cells less susceptible to productive infection.

Animals↗
PubMed2004

Down-regulation of matrix-invasive potential of human liver cancer cells by type I interferon and a histone deacetylase inhibitor sodium butyrate.

We have demonstrated anti-proliferation and anti-metastasis effects of both interferon-alpha and a histone deacetylase inhibitor, sodium butyrate, on human liver cancer cell lines. In this study, invasive ability of human liver cancer cell lines through the matrix-coated membrane was examined and inhibitory effect of interferon-alpha and sodium butyrate was investigated. Among six human liver cancer cell lines, HLE and HLF showed high invasive ability using the Matrigel invasion assay. This invasion ability was significantly inhibited by pretreatment of the cells with 1000 IU/ml of interferon-alpha or 2 mM of sodium butyrate. Gelatin zymography and the matrix metalloproteinase-2 and -9 activity assay showed that these two cell lines produce active- and pro-matrix metalloproteinase-2 and -9, and their activity was significantly reduced by pretreatment with both agents. Real-time quantitative reverse transcription-polymerase chain reaction showed decrease in matrix metalloproteinase-1 mRNA levels by pretreatment with both agents, but mRNA levels of tissue inhibitor of matrix metalloproteinase-1 and -2 were differently modulated by interferon-alpha and sodium butyrate. These results suggest that interferon-alpha and sodium butyrate reduce a chance of invasion and metastasis of human liver cancer cells by inhibiting matrix metalloproteinase activity, although its inhibitor is differently regulated.

Antineoplastic Agents↗
PubMed1986

[Effect of different types of interferon on the natural cellular cytotoxicity of lung cancer patients].

The natural killer cell cytotoxicity was studied in the 4 hour and 18 hour cytotoxic reaction with cultured human tumour cells (K562 and lung adenocarcinoma) labelled by 51Cr. The natural killer cell activity of cancer patients was lowered only in 4 hour cytotoxic reaction with target cells K562. The natural and recombinant leucocyte interferon and natural immune interferon stimulated in vitro the activity of natural killer cells in most of the experiments (80.5 %) in the 4 hour and 18 hour cytotoxic reactions both from patients with initially lowered level, and with normal or high level of cytotoxic action of natural killer cells. In some experiments interferon preparations did not significantly influence the lysis of tumour cells or even suppressed the activity of effector cells. The heterogeneity of the population of natural killer cells and different immunomodulating effects of interferon were discussed.

Adenocarcinoma↗
PubMed1980

Factors affecting the assay of bovine type I interferon on bovine embryonic lung cells.

One preparation of interferon (IF) on 7-day-old bovine embryonic lung cultures free of bovine viral diarrhea virus had titers ranging from 20 to 10,240 in plaque-reduction tests, using bovine vesicular stomatitis virus. Factors believed to contribute to this variation were investigated. Although titers differed on different cell strains, different passages, and on cultures of different ages, variations between the two assays definitely could not be established as a function of these factors. However, IF titers on low passage cultures were usually lower than were titers on subsequent passages of the same cell strain. Calf serum in the diluent for IF reduced the titer one or two twofold dilutions. Over the range of 7 to 24 hours contact of IF with bovine embryonic lung cultures, and titer decreased steadily and was one twofold dilution less at 24 hours than it was at 7 hours. Latent viruses were not found in cultures by electron microscopy. Treatment of cultures with a noncytopathogenic strain of bovine viral diarrhea virus almost eliminated the effect of IF. Naturally occurring production of IF was not a major problem. While IF was on the cells, the pH of IF had a pronounced effect on the titer and may have been responsible for the vatiation observed with different passages, different cell strains, use of cultures of different ages, and use of calf serum in the diluent. Interferon at a low pH had a titer three or four twofold dilutions less than did the IF at a high pH.

Animals↗
PubMed1980

Factors affecting the production of bovine type I interferon on bovine embryonic lung cells by polyriboinosinic-polyribocytidylic acid.

Variables believed to affect the amount of interferon (IF) produced in bovine embryonic lung cell cultures by polyriboinosinic-polyribocytidylic acid (poly (rI:rC)) were investigated. A concentration of 100 micron of poly (rI:rC)/ml consistently induced substantial amounts of IF. Bovine viral diarrhea virus infection of cultures did not interfere with induction of IF by poly (rI:rC). Neither the age of cells nor the passage level of the cultures seemed to affect the amount of IF produced. Priming of cultures with large concentrations of IF before treatment with poly (rI:rC) was more effective than priming with small concentrations of IF. Furthermore, priming for 24 hours was more effective than was priming for 12 hours. The use of 2% bovine fetal serum in the medium, subsequent to treatment with poly (rI:rC) markely enhanced IF production. Practically all IF was produced within a few hours after treatment with poly (rI:rC).

Animals↗
PubMed1989

[Interferon in the modulation of the immune response in pyelonephritis caused by Staphylococci and Pseudomonas aeruginosa].

In experiments on mice the influence of mouse serum interferon, type I, on immune response in pyelonephritis caused by staphylococci and P. aeruginosa has been studied. The immunomodulating action of interferon and its therapeutic effectiveness have been shown to depend on the etiology of the disease. When injected intraperitoneally in a dose of 1,000 ED, interferon produces a pronounced therapeutic effect in pyelonephritis caused by P. aeruginosa and no effect in pyelonephritis of staphylococcal etiology. Type I interferon introduced in the dose used in this investigation has no influence on the killer activity of spleen lymphocytes, enhances the activity of the complement and the production of antibodies, produces a leukopenic effect and, depending on the etiology of pyelonephritis, exerts influence on the activity of dehydrogenases, the number of EAC- and E-rosette-forming cells, the oxidation metabolism of neutrophils and their phagocytic activity.

Animals↗
PubMed2005

Resistance of paramyxoviridae to type I interferon-induced Bos taurus Mx1 dynamin.

Typical targets of type I interferon (IFN)-induced antiviral Mx proteins known to date have been shown to share a common profile: single-stranded negative-sense RNA viruses. Among them, human MxA is known to interfere with the replication of measles, human, and bovine parainfluenza-3 viruses (BoPi3V), that is, three members of the Paramyxoviridae family. Recently, bovine Mx1 protein (BoMx1) was included in the group of Mx proteins with authenticated antiviral potential, as it dramatically represses the replication of vesicular stomatitis virus (VSV). As replication in bovine cells of Pi3, respiratory syncytial (RS), and Sendai (Se) viruses, all members of the same family, is known to be reduced on IFN-alpha incorporation into the culture medium, it was hypothesized that the BoMx1 pathway possibly was involved, its antiviral spectrum thus probably extending to Paramyxoviridae. In this study, probing of BoMx1-inhibiting effects was carried out by infecting a transgenic Vero cell line that allows tightly regulated conditional expression of BoMx1 after doxycycline treatment with a wide array of Paramyxoviridae. Expressing and nonexpressing cells displayed similar viability, cytopathic effects (CPEs), and amounts of infectious virus yields, whatever the infecting virus or the multiplicity of infection (moi) imposed. It is, therefore, concluded that BoMx1 does not interfere with Paramyxoviridae.

Animals↗
PubMed2004

[Development of binding antibodies to interferon-beta during treatment of multiple sclerosis with different types of interferon-beta].

Interferon beta (IFN-beta) is generally considered an effective treatment for multiple sclerosis (MS). Importance of binding antibodies (BAb), which are created during the treatment of MS by the use of IFN-beta, hasn't been completely explained, however it is generally reckoned that they might be one of the factors diminishing treatment efficacy. The aim of the study was the appreciation of BAb occurrence during the treatment of MS by the use of different types of interferon beta and their impact on clinical efficacy. The study included 47 patients with relapsing-remitting MS. Within 24 months 37 patients were given two different preparations of IFN-beta 1-a and 10 patients were given IFN-beta 1-b. Every 6 months clinical parameters and BAb level in serum by EIA method were estimated. All preparations of IFN-beta induced appearance of BAb, but frequency of developing BAb to IFN-beta varied according to the IFN beta given. The high levels of BAb appeared significant frequently in patients treated with IFN-beta 1-b than in patients treated with both preparations of IFN-beta 1-a. After 2 years of treatment greater disability, measured by EDSS scale was encountered in patients with high levels of BAb but differences weren't statistically significant. As well, it wasn't stated significant correlation between exacerbation numbers during the treatment.

Adjuvants, Immunologic↗
PubMedDate not supplied

Control of the interferon system: an inhibitor of interferon action.

An inhibitor of interferon action has been identified which is present in IFN-gamma preparations. The inhibitor is produced following rising interferon concentrations in mitogen stimulated mouse spleen cell cultures. Indications are that the inhibitor is produced in response to the production of interferon, and may therefore be a feedback control mechanism for the interferon system. The action of the inhibitor is independent of both interferon type and concentration, and seems to act by preventing the establishment of the interferon-induced antiviral state at some point following the interaction of the interferon molecule with the cell membrane. The inhibitor has an apparent molecular weight of 8,000 to 10,000 daltons and is stable to treatment with low pH, heat, and trypsin. It is proposed that the inhibitor has the specific role in vivo of controlling interferon-mediated activities.

Animals↗
PubMed2004

The Jak-STAT pathway stimulated by interferon alpha or interferon beta.

Type I interferons, such as interferon alpha and interferon beta (IFN-alpha and beta), signal through a Janus kinase (Jak) to signal transduction and activator of transcription (STAT) pathway to stimulate gene expression. In response to ligand binding, the receptors dimerize, Jaks phosphorylate STAT1 and STAT2, which then dimerize and interact with a third transcriptional regulator IFN regulatory factor 9 (IRF9) to stimulate gene expression. IFN-alpha is the main innate antiviral cytokine and is essential for effective immune response to viral infection. The animation shows activation of STAT-responsive gene expression in response to type I IFNs.

DNA-Binding Proteins↗
PubMedDate not supplied

[The antiproliferative effects associated with vincristine and human interferons in experimental in vitro systems].

Cytotoxic potential of suboptimal doses of vincristine associated with human interferon was studied in two cell lines of tumoral origin, as compared to the action of or gamma type interferon preparations. Results show that the vincristine cytotoxic effect may be synergistically augmented in both culture types by simultaneous interferon administration.

Cell Division↗