Search results for "Interferon-beta"

showing 5 items of 35 documents

TLR4 abrogates the Th1 immune response through IRF1 and IFN-β to prevent immunopathology during L. infantum infection

2020

A striking feature of human visceral leishmaniasis (VL) is chronic inflammation in the spleen and liver, and VL patients present increased production levels of multiple inflammatory mediators, which contribute to tissue damage and disease severity. Here, we combined an experimental model with the transcriptional profile of human VL to demonstrate that the TLR4-IFN-β pathway regulates the chronic inflammatory process and is associated with the asymptomatic form of the disease. Tlr4-deficient mice harbored fewer parasites in their spleen and liver than wild-type mice. TLR4 deficiency enhanced the Th1 immune response against the parasite, which was correlated with an increased activation of de…

PhysiologyGene ExpressionWhite Blood CellsMiceCell SignalingAnimal CellsImmune PhysiologyZoonosesImmunopathologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Immune ResponseLeishmaniasisProtozoansLeishmaniaMice Knockout0303 health sciencesbiologyT Cells030302 biochemistry & molecular biologyEukaryotaImmune Receptor SignalingInfectious Diseasesmedicine.anatomical_structureLeishmaniasis VisceralCellular Typesmedicine.symptomLeishmania infantumResearch ArticleSignal TransductionNeglected Tropical DiseasesQH301-705.5Leishmania InfantumImmune CellsImmunologySpleenInflammationLEISHMANIOSE VISCERALMicrobiology03 medical and health sciencesImmune systemVirologyParasitic DiseasesGeneticsmedicineAnimalsMolecular Biology030304 developmental biologyInflammationProtozoan InfectionsBlood CellsOrganismsBiology and Life SciencesCell BiologyInterferon-betaTh1 CellsRC581-607Tropical Diseasesmedicine.diseasebiology.organism_classificationParasitic ProtozoansToll-Like Receptor 4IRF1Visceral leishmaniasisImmunologyTLR4ParasitologyImmunologic diseases. AllergySpleenInterferon Regulatory Factor-1
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Treatment of multiple sclerosis with interferon beta in clinical practice: 2-year follow-up data from the South Italy Mobile MRI Project.

2006

This follow-up study assessed the 2-year clinical and magnetic resonance imaging (MRI) outcomes of patients with multiple sclerosis (MS) originally enrolled in an MRI study conducted at eight centres in south Italy (the South Italy Mobile MRI Project). Of the 597 MS patients recruited at baseline, 391 returned for the follow-up study. Of these, 363 provided 2-year clinical and MRI follow-up data, and 215 were still undergoing treatment with one of four interferon beta regimens: Avonex, 30 mcg intramuscularly once weekly; Betaferon, 250 mcg subcutaneously (sc) every other day; Rebif 22 mcg sc three times weekly (tiw; Rebif 22); or Rebif 44 mcg sc tiw (Rebif 44). Over the 2-year follow-up per…

medicine.medical_specialtyNeurologyMultiple SclerosisDermatologySeverity of Illness IndexInterferon beta • Multiple sclerosis • Phase IV • Odds ratioInternal medicineSeverity of illnessmedicineConfidence IntervalsHumansImmunologic FactorsMultiple sclerosiNeuroradiologyAnalysis of Variancemedicine.diagnostic_testbusiness.industryMultiple sclerosisMagnetic resonance imagingGeneral MedicineOdds ratioInterferon-betaOdds ratiomedicine.diseaseInterferon betaMagnetic Resonance ImagingConfidence intervalPsychiatry and Mental healthItalyPhysical therapySettore MED/26 - NeurologiaNeurology (clinical)NeurosurgeryPhase IVbusinessFollow-Up Studies
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Rac1 and PAK1 are upstream of IKK-ε and TBK-1 in the viral activation of interferon regulatory factor-3

2004

The anti-viral type I interferon (IFN) response is initiated by the immediate induction of IFN beta, which is mainly controlled by the IFN-regulatory factor-3 (IRF-3). The signaling pathways mediating viral IRF-3 activation are only poorly defined. We show that the Rho GTPase Rac1 is activated upon virus infection and controls IRF-3 phosphorylation and activity. Inhibition of Rac1 leads to reduced IFN beta promoter activity and to enhanced virus production. As a downstream mediator of Rac signaling towards IRF-3, we have identified the kinase p21-activated kinase (PAK1). Furthermore, both Rac1 and PAK1 regulate the recently described IRF-3 activators, I kappa B kinase- and TANK-binding kina…

rac1 GTP-Binding ProteinTranscription GeneticBiophysicsIκB kinaseProtein Serine-Threonine KinasesSignal transductionBiologyVirus ReplicationBiochemistryCell LineDogsPAK1Structural BiologyInterferonGeneticsmedicineAnimalsHumansPhosphorylationPromoter Regions Geneticp21-activated kinasesMolecular BiologyRNA Double-StrandedKinaseRho GTPaseI-Kappa-B KinaseNuclear ProteinsInterferon-betaCell BiologyCREB-Binding ProteinI-kappa B KinaseDNA-Binding ProteinsEnzyme Activationp21-Activated KinasesInfluenza A virusViral infectionAnti-viral responseTrans-ActivatorsCancer researchInterferon Regulatory Factor-3Transcription factorSignal transductionDimerizationTranscription FactorsInterferon regulatory factorsmedicine.drugFEBS Letters
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Off-Adherence Keeping (OAK) observational study: intentional off-adherence immunomodulatory multiple sclerosis treatment

2022

Aims: To evaluate how improved treatment adherence with a lower-frequency regimen/treatment of intramuscular (IM) IFN beta-1a impacts therapeutic effectiveness in relapsing-remitting multiple sclerosis (MS) patients switching from a higher-frequency injectable regimen/treatment. Patients & methods: Italian patients with relapsing-remitting MS and prior poor adherence to high-frequency injectable treatments (n = 181) were followed for 24 months after starting IM IFN beta-1a. Results: During the study, 97.4% of patients were treatment adherent; 22.1% of patients reported a relapse. The estimated probability of remaining relapse-free after 2 years was 78%. A high dropout rate (52.5%) led t…

relapsesMultiple Sclerosis Relapsing-RemittingTreatment Outcomequality of lifeRecurrenceHumansSettore MED/26 - NeurologiaInterferon-betaNeurology (clinical)multiple sclerosistreatment adherenceInterferon beta-1aintramuscular interferon beta-1aNeurodegenerative Disease Management
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Enhancement by TNF-alpha of reactivation and replication of latent herpes simplex virus from trigeminal ganglia of mice.

1995

The influence of tumor-necrosis-factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukine-1 (IL-1) and IL-3 on the in vitro reactivation frequency and replication rate of trigeminal ganglia of mice latently infected with herpes simplex virus (HSV) strain KOS was studied. It could be demonstrated that TNF-alpha and possibility GM-CSF, but not IL-1 and IL-3, enhanced the reactivation frequency and replication of HSV. Interferon alpha/beta (IFN alpha/beta) prevented reactivation and replication.

virusesmedicine.medical_treatmentHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationVirusHerpesviridaeMiceInterferonVirologyAlphaherpesvirinaeChlorocebus aethiopsmedicineAnimalsHumansVero CellsMice Inbred BALB CTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaGeneral MedicineInterferon-betabiology.organism_classificationVirologyIn vitroVirus LatencyCytokineHerpes simplex virusViral replicationTrigeminal GanglionInterleukin-3Virus Activationmedicine.drugInterleukin-1Archives of virology
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