Search results for "Tumor necrosis factor-alpha"

showing 10 items of 504 documents

Dose adjustments and discontinuation in TNF inhibitors treated patients: when and how. A systematic review of literature.

2018

Objectives To review the available evidence concerning the possibility of discontinuing and/or tapering the dosage of TNF inhibitors (TNFi) in RA patients experiencing clinical remission or low disease activity. Methods A systematic review of the literature concerning the low dosage and discontinuation of TNFi in disease-controlled RA patients was performed by evaluation of reports published in indexed international journals (Medline via PubMed, EMBASE), in the time frame from 8 April 2013 to 15 January 2016. Results We analysed the literature evaluating the efficacy and the safety of two different strategies using TNFi, decreasing dosage or discontinuation, in patients experiencing clinica…

Drugmedicine.medical_specialtymedia_common.quotation_subjectMEDLINEArthritisEtanerceptDose-Response RelationshipArthritis Rheumatoid03 medical and health sciences0302 clinical medicineRheumatologyRheumatoidInternal medicinemedicineAdalimumabHumansPharmacology (medical)030212 general & internal medicinemedia_common030203 arthritis & rheumatologyDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaArthritisRemission Inductionmedicine.diseaseRheumatologyAntirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Humans; Remission Induction; Tumor Necrosis Factor-alpha; Rheumatology; Pharmacology (medical)DiscontinuationRheumatoid arthritisAntirheumatic AgentsDrugbusinessmedicine.drugRheumatology (Oxford, England)
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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Endothelin-1 modulates the expression of adhesion molecules on fibroblast-like synovial cells (FLS)

1996

Endothelin-1 is known to possess various biological properties. In the present study we have investigated the effects of Endothelin-1 (Et-1) on the expression of adhesion molecules ICAM-1, VCAM-1 and CD-44 by fibroblast-like synoviocytes. Cultured fibroblast-like synoviocytes were treated with Et-1 in the absence or presence of C1306, a specific endothelin-A-receptor antagonist. Cell surface expression of ICAM-1, VCAM-1 and CD-44 was determined by immunofluorescence studies, Cyto-ELISA and FACS-analysis. ICAM-1, VCAM-1 and CD-44 were constitutively expressed on cultured FLS. After incubation with Et-1 the expression of ICAM-1, VCAM-1 and CD-44 increased. The level of expression of adhesion …

Endothelin Receptor Antagonistsmedicine.medical_specialtymedicine.medical_treatmentImmunologyVascular Cell Adhesion Molecule-1BiologyProinflammatory cytokineRheumatologyDownregulation and upregulationInternal medicinemedicineHumansImmunology and AllergyCells CulturedEndothelin-1Tumor Necrosis Factor-alphaCell adhesion moleculeSynovial MembraneGeneral MedicineAdhesionFibroblastsIntercellular Adhesion Molecule-1Receptor Endothelin AIn vitroCell biologyHyaluronan ReceptorsCytokinemedicine.anatomical_structureEndocrinologyCell cultureSynovial membraneCell Adhesion MoleculesInterleukin-1
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Differential effects of anti-TNF-α and anti-IL-12/23 agents on human leukocyte–endothelial cell interactions

2015

AbstractEnhanced leukocyte recruitment is an inflammatory process that occurs during early phases of the vascular dysfunction that characterises atherosclerosis. We evaluated the impact of anti-TNF-α (adalimumab, infliximab and etanercept) and anti-IL-12/23 (ustekinumab) on interactions between human leukocytes and endothelial cells in a flow chamber that reproduced in vivo conditions. Clinical concentrations of anti-TNF-α were evaluated on the leukocyte recruitment induced by a variety of endothelial (TNF-α, interleukin-1β, lymphotoxin-α and angiotensin-II) and leukocyte (PAF, IL-12 and IL-23) stimuli related to inflammation and atherosclerosis. Treatment with anti-TNF-α, even before or af…

EndotheliumInflammationAnti-IL-12/23 agentsCardiovascular side effectsBiologicsInterleukin-23Rheumatic diseasesIn vivoPsoriasisHuman Umbilical Vein Endothelial CellsInterleukin 23HumansMedicineAnti-TNF-α agentsPharmacologyTumor Necrosis Factor-alphabusiness.industryCell adhesion moleculeAdalimumabEndothelial Cellsmedicine.diseaseInterleukin-12Leukocyte–endothelial cell interactionsEndothelial stem cellmedicine.anatomical_structureImmunologyLeukocytes MononuclearTumor necrosis factor alphamedicine.symptombusinessEuropean Journal of Pharmacology
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Role for Tumor Necrosis Factor Alpha in Murine Cytomegalovirus Transcriptional Reactivation in Latently Infected Lungs

2004

ABSTRACT Interstitial pneumonia is a major clinical manifestation of primary or recurrent cytomegalovirus (CMV) infection in immunocompromised recipients of a bone marrow transplant. In a murine model, lungs were identified as a prominent site of CMV latency and recurrence. Pulmonary latency of murine CMV is characterized by high viral genome burden and a low incidence of variegated immediate-early (IE) gene expression, reflecting a sporadic activity of the major IE promoters (MIEPs) and enhancer. The enhancer-flanking promoters MIEP1/3 and MIEP2 are switched on and off during latency in a ratio of ∼2:1. MIEP1/3 latency-associated activity generates the IE1 transcript of the ie1/3 transcrip…

Gene Expression Regulation ViralHuman cytomegalovirusMuromegalovirusTranscription GeneticImmunologyBiologyMicrobiologyImmediate early proteinImmediate-Early ProteinsMiceViral ProteinsTransactivationVirologyGene expressionVirus latencymedicineAnimalsHumansEnhancerLungBone Marrow TransplantationMice Inbred BALB CTumor Necrosis Factor-alphaAlternative splicingPromoterHerpesviridae Infectionsmedicine.diseaseVirologyVirus LatencyVirus-Cell InteractionsDisease Models AnimalTransplantation IsogeneicInsect ScienceFemaleVirus ActivationJournal of Virology
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Chronic inflammatory cardiomyopathy of interferon γ-overexpressing transgenic mice is mediated by tumor necrosis factor-α.

2011

We recently described a model of inflammatory cardiomyopathy in interferon (IFN)-γ overexpressing transgenic mice stably circulating IFN-γ in the serum referred to as SAP–-IFN-γ mice. SAP–IFN-γ transgenic mice show cardiac infiltration by mononuclear leukocytes, culminating in dilated cardiomyopathy characterized by an increase of left ventricular end diastolic diameter and reduction of fractional shortening. We hypothesized that the pathological mechanism underlying SAP–IFN-γ cardiomyopathy might be mediated by (auto)immune processes or tumor necrosis factor (TNF)-α synthesis from IFN-γ–activated macrophages. To verify these hypotheses, we crossed SAP–IFN-γ transgenic mice with immunodefic…

Genetically modified mouseMalemedicine.medical_specialtyMyocarditisTransgeneCardiomyopathyApoptosisAutoimmunityMice TransgenicKaplan-Meier EstimateBiologyAdaptive ImmunityPathology and Forensic MedicineHepatitisInterferon-gammaMiceImmune systemInterferonInternal medicinemedicineAnimalsGene SilencingTumor Necrosis Factor-alphaMacrophagesAlanine Transaminasemedicine.diseaseMyocarditisEndocrinologyPhenotypeEchocardiographyKnockout mouseChronic DiseaseCytokinesTumor necrosis factor alphaFemalemedicine.drugThe American journal of pathology
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Severe hepatic injury in interleukin 18 (IL-18) transgenic mice: a key role for IL-18 in regulating hepatocyte apoptosis in vivo.

2004

Background: Interleukin 18 (IL-18) is a cytokine with pleiotropic activity that augments T helper 1 responses and cytotoxic activity of natural killer cells. Methods: To assess the function of IL-18 in vivo, we generated IL-18 transgenic (IL-18 Tg) mice under the control of a CD2 promoter/enhancer construct. Results: Macroscopically, IL-18 Tg mice showed reduced relative liver weight compared with wild-type littermates. TUNEL assays demonstrated increased hepatocyte apoptosis, and primary hepatocytes isolated from IL-18 Tg mice exhibited an increased spontaneous apoptosis rate. Furthermore, cross linking of Fas increased significantly the apoptosis rate in hepatocytes isolated from wild- ty…

Genetically modified mousemedicine.medical_specialtyTransgeneT-LymphocytesApoptosisMice TransgenicMice SCIDBiologyTransfectionTranslocation GeneticInterferon-gammaMiceIn vivoInternal medicinemedicineCytotoxic T cellAnimalsfas ReceptorL-SelectinCells CulturedLiver injuryTumor Necrosis Factor-alphaGastroenterologyInterleukin-18NF-kappa BOrgan Sizemedicine.diseaseAdoptive TransferEndocrinologymedicine.anatomical_structureLiverApoptosisHepatocyteLymphocyte TransfusionCancer researchHepatocytesInterleukin 18Gut
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HBV-specific immune defect in chronic hepatitis B (CHB) is correlated with a dysregulation of pro- and anti-inflammatory cytokines.

1999

SUMMARY The aim of this study was to examine the immunomodulating effects of rhIL-12 on the immune response induced by hepatitis B virus (HBV) antigens in clinical subgroups of patients with HBV infection. Peripheral blood mononuclear cells (PBMC) of 80 patients were stimulated with HBsAg, HBcAg, pre-S1Ag and tetanus toxoid in the absence or presence of IL-12 (0.01, 0.1 and 1 ng/ml). Stimulation by anti-CD3 + anti-CD28 and lipopolysaccharide (LPS) were used as controls. Proliferation and cytokine production were determined by 3H-thymidine uptake and ELISA after 72 h. After stimulation with HBV antigens only, production of tumour necrosis factor-alpha (TNF-α) or IL-10 was observed in all pat…

HBsAgHepatitis B virusImmunologyAntigen-Presenting CellsIn Vitro Techniquesmedicine.disease_causeLymphocyte ActivationHepatitis B AntigensInterferon-gammaHepatitis B ChronicOrthohepadnavirusmedicineImmunology and AllergyHumansHepatitis B AntibodiesHepatitisHepatitis B virusbiologybusiness.industryTumor Necrosis Factor-alphavirus diseasesOriginal ArticlesHepatitis Bmedicine.diseasebiology.organism_classificationVirologyInterleukin-12digestive system diseasesRecombinant ProteinsInterleukin-10HBcAgHBeAgHepadnaviridaeImmunologyDNA ViralLeukocytes MononuclearCytokinesInflammation MediatorsbusinessClinical and experimental immunology
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Effects of tumor necrosis factor-alpha on tumor blood flow and hyperthermic treatment.

1989

The impact of recombinant human tumor necrosis factor-alpha (rhTNF-alpha), given alone or in combination with local hyperthermia, on perfusion and growth of a moderately rhTNF-alpha-sensitive rat tumor (DS-carcinosarcoma) was investigated. DS-carcinosarcomas were implanted into the hind foot dorsum of Sprague-Dawley rats. Tumor blood flow (TBF) was measured with the krypton-85 clearance technique. Treatment with either tumor necrosis factor-alpha (0.1-1.0 mg/kg) or hyperthermia (43.3 and 44.3 degrees C, 40 min) can decrease the perfusion of malignant tumors. The TBF reduction was fully established 2 h after rhTNF-alpha injection and lasted for at least 4 h. The application of local hyperthe…

HyperthermiaCancer ResearchNecrosisSoft Tissue NeoplasmsPharmacologyCarcinosarcomaTumor perfusionmedicineAnimalsTumor growthTumor necrosis factor αbusiness.industryTumor Necrosis Factor-alphaRats Inbred StrainsHematologyBlood flowHyperthermia Inducedmedicine.diseaseCombined Modality TherapyRecombinant ProteinsRatsOncologyRegional Blood FlowImmunologyTumor necrosis factor alphamedicine.symptombusinessPerfusionCell DivisionNeoplasm TransplantationOnkologie
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In vivo targets of recombinant human tumour necrosis factor-α: blood flow, oxygen consumption and growth of isotransplanted rat tumours

1989

The impact of recombinant human tumour necrosis factor-alpha (1 microgram kg-1 to 1 mg kg-1; 6.6 x 10(6) U mg protein-1) on blood flow, oxygen consumption and growth of a moderately TNF-sensitive rat tumour (DS-carcinosarcoma) was studied. Tumour growth was stimulated at low TNF doses (1 and 10 micrograms kg-1) and significantly retarded at higher TNF dose levels (0.1 and 1 mg kg-1). Growth changes were concomitant with variations in oxygen consumption, lactate release and acidification of the metabolic micromilieu. Both single and repeated application of low TNF doses (1-10 micrograms kg-1 i.v.) increased tumour perfusion whereas single administration of high TNF dose levels (0.1-1 mg kg-1…

HyperthermiaCancer Researchmedicine.medical_specialtyNecrosismedicine.medical_treatmentBiologyOxygen ConsumptionCarcinosarcomaIn vivoInternal medicinemedicineAnimalsChemotherapyTumor Necrosis Factor-alphaCell growthAscitesRats Inbred StrainsBlood flowmedicine.diseaseRecombinant ProteinsRatsEndocrinologyOncologyRegional Blood FlowTumor necrosis factor alphamedicine.symptomPerfusionNeoplasm TransplantationResearch ArticleBritish Journal of Cancer
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