Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

A20 expression in dendritic cells protects mice from LPS-induced mortality

2014

DCs contribute to immune homeostasis under physiological conditions and regulate the immune activation during infection. The deubiquitinase A20 inhibits the activation of NF-κB-dependent immune reactions, and prevents the hyperactivation of DCs under steady-state conditions. However, the role of DC-specific A20 under pathological conditions is unknown. Here, we demonstrate that upon injection of low-dose LPS, mice with DC-specific A20 deletion (CD11c-Cre A20(fl/fl) ) died within 6 h, whereas A20(fl/fl) controls survived. LPS-induced mortality in CD11c-Cre A20(fl/fl) mice was characterized by increased serum levels of IL-2, IL-10, IL-12, IFN-γ, and TNF. Upon LPS stimulation, the activation o…

MAPK/ERK pathwayRegulation of gene expressionImmunologychemical and pharmacologic phenomenaStimulationTumor Necrosis Factor alpha-Induced Protein 3Biologymedicine.disease_causeIn vitroAutoimmunityimmune system diseasesIn vivohemic and lymphatic diseasesImmunologymedicineImmunology and AllergyTumor necrosis factor alphaEuropean Journal of Immunology
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Granulocyte-macrophage colony-stimulating factor induces cytokine secretion by human polymorphonuclear leukocytes.

1989

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous…

Macrophage colony-stimulating factorNeutrophilsT cellInflammationBiologyBiological FactorsMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineAnimalsHumansRNA MessengerGrowth SubstancesTumor Necrosis Factor-alphaMacrophage Colony-Stimulating FactorLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGeneral MedicineColony-stimulating factorRecombinant ProteinsRetractionCell biologymedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyCytokinesTumor necrosis factor alphaCytokine secretionmedicine.symptomResearch Articlemedicine.drugJournal of Clinical Investigation
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Tumor necrosis factor (TNF)-alpha but not TNF-beta induces secretion of colony stimulating factor for macrophages (CSF-1) by human monocytes

1987

Abstract Tumor necrosis factor (TNF)-alpha has been identified as a major inducer of colony stimulating factor (CSF)-secretion by human vascular endothelial cells and fibroblasts. In the present study we assessed the capacity of TNFs to induce release of CSF-1 from highly purified peripheral blood monocyte preparations. Whereas monocytes do not accumulate CSF-1 messenger (m)RNA constitutively and consequently do not produce CSF-1 protein, CSF-1 mRNA and protein secretion became detectable, when monocytes were cultured in the presence of TNF-alpha, that was synergistically enhanced by interferon-gamma (IFN-gamma). However, under identical experimental conditions TNF-beta failed to induce mon…

Macrophage colony-stimulating factormedicine.medical_specialtyT-LymphocytesImmunologyIn Vitro TechniquesBiologyBiochemistryMonocytesColony-Forming Units AssayColony-Stimulating FactorsInternal medicinemedicineHumansSecretionLeukapheresisMessenger RNATumor Necrosis Factor-alphaMonocyteCell BiologyHematologyMacrophage ActivationColony-stimulating factorMolecular biologyHaematopoiesisEndocrinologySecretory proteinmedicine.anatomical_structureTumor necrosis factor alphaBlood
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Interleukin-17 Inhibition in Spondyloarthritis Is Associated With Subclinical Gut Microbiome Perturbations and a Distinctive Interleukin-25-Driven In…

2020

Objective To characterize the ecological effects of biologic therapies on the gut bacterial and fungal microbiome in psoriatic arthritis (PsA)/spondyloarthritis (SpA) patients. Methods Fecal samples from PsA/SpA patients pre- and posttreatment with tumor necrosis factor inhibitors (TNFi; n = 15) or an anti-interleukin-17A monoclonal antibody inhibitor (IL-17i; n = 14) underwent sequencing (16S ribosomal RNA, internal transcribed spacer and shotgun metagenomics) and computational microbiome analysis. Fecal levels of fatty acid metabolites and cytokines/proteins implicated in PsA/SpA pathogenesis or intestinal inflammation were correlated with sequence data. Additionally, ileal biopsies obtai…

Male0301 basic medicineArthritisPsoriatic0302 clinical medicineInterleukin 25Monoclonal2.1 Biological and endogenous factorsImmunology and AllergyMedicineAetiologyIntestinal MucosaCandida albicansHumanizedSubclinical infectionbiologyInterleukin-17Innate lymphoid cellMiddle AgedIntestinesPublic Health and Health ServicesFemaleTumor necrosis factor alphaInterleukin 17Clinical SciencesImmunologyAntibodies Monoclonal HumanizedAutoimmune DiseaseAntibodiesArticle03 medical and health sciencesRheumatologyClinical ResearchSpondylarthritisHumansMicrobiomeInflammation030203 arthritis & rheumatologybusiness.industryArthritisInflammatory and immune systemArthritis Psoriaticbiology.organism_classificationmedicine.diseaseArthritis & RheumatologyGastrointestinal Microbiome030104 developmental biologyImmunologyTumor Necrosis Factor InhibitorsDigestive Diseasesbusiness
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Fibroblast Growth Factor 21 (FGF21) Protects against High Fat Diet Induced Inflammation and Islet Hyperplasia in Pancreas

2015

Fibroblast growth factor 21 (FGF21) is an important endocrine metabolic regulator expressed in multiple tissues including liver and adipose tissue. Although highest levels of expression are in pancreas, little is known about the function of FGF21 in this tissue. In order to understand the physiology of FGF21 in the pancreas, we analyzed its expression and regulation in both acinar and islet tissues. We found that acinar tissue express 20-fold higher levels than that observed in islets. We also observed that pancreatic FGF21 is nutritionally regulated; a marked reduction in FGF21 expression was noted with fasting while obesity is associated with 3–4 fold higher expression. Acinar and islet c…

Male0301 basic medicineFGF21Fibroblast Growth FactorPhysiologyReceptors Antigen T-Cell alpha-betaPeptide Hormoneslcsh:MedicineAdipose tissueAcinar CellsPathology and Laboratory MedicineBiochemistryFatsMiceEndocrinologyMedicine and Health SciencesInsulinlcsh:ScienceImmune ResponseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Multidisciplinarygeography.geographical_feature_categoryFOXP3Forkhead Transcription FactorsFastingHyperplasiaIsletLipidsmedicine.anatomical_structurePhysiological ParametersOrgan SpecificityTumor necrosis factor alphaAnatomymedicine.symptomPancreasSignal TransductionResearch Articlemedicine.medical_specialtyImmunologyEndocrine SystemInflammationBiologyDiet High-FatInterferon-gammaIslets of Langerhans03 medical and health sciencesExocrine GlandsSigns and SymptomsGrowth FactorsInternal medicinemedicineAnimalsObesityPancreasNutritionInflammationDiabetic EndocrinologygeographyHyperplasiaEndocrine PhysiologyTumor Necrosis Factor-alphaBody Weightlcsh:RBiology and Life SciencesGlucagonmedicine.diseaseDietary FatsHormonesDietFibroblast Growth FactorsMice Inbred C57BL030104 developmental biologyEndocrinologyGene Expression RegulationPancreatitisThy-1 Antigenslcsh:QPLOS ONE
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Canakinumab for the Treatment of Autoinflammatory Recurrent Fever Syndromes.

2018

BACKGROUND: Familial Mediterranean fever, mevalonate kinase deficiency (also known as the hyperimmunoglobulinemia D syndrome), and the tumor necrosis factor receptor-associated periodic syndrome (TRAPS) are monogenic autoinflammatory diseases characterized by recurrent fever flares. METHODS: We randomly assigned patients with genetically confirmed colchicine-resistant familial Mediterranean fever, mevalonate kinase deficiency, or TRAPS at the time of a flare to receive 150 mg of canakinumab subcutaneously or placebo every 4 weeks. Patients who did not have a resolution of their flare received an add-on injection of 150 mg of canakinumab. The primary outcome was complete response (resolution…

Male0301 basic medicineInterleukin-1betaFamilial Mediterranean fever0302 clinical medicineMonoclonalChildMedicine(all)Mevalonate kinase deficiencySubcutaneousMedicine (all)Interleukin-1betaAntibodies MonoclonalGeneral MedicineFamilial Mediterranean FeverRecurrent feverChild PreschoolFemaleTumor necrosis factor alphaDrugInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]medicine.drugAdultAdolescentFeverInjections SubcutaneousHereditary Autoinflammatory DiseasesAntibodies Monoclonal HumanizedAdolescent; Adult; Antibodies Monoclonal/administration & dosage; Antibodies Monoclonal/adverse effects; Antibodies Monoclonal/therapeutic use; Child; Child Preschool; Dose-Response Relationship Drug; Double-Blind Method; Familial Mediterranean Fever/drug therapy; Female; Fever/drug therapy; Hereditary Autoinflammatory Diseases/drug therapy; Humans; Injections Subcutaneous; Interleukin-1beta/antagonists & inhibitors; Male; Mevalonate Kinase Deficiency/drug therapy; Young AdultAntibodiesInjectionsDose-Response RelationshipYoung Adult03 medical and health sciencesAll institutes and research themes of the Radboud University Medical CenterDouble-Blind MethodGeneral & Internal MedicinemedicineHumansPreschoolAdolescent; Adult; Antibodies Monoclonal; Child; Child Preschool; Dose-Response Relationship Drug; Double-Blind Method; Familial Mediterranean Fever; Female; Fever; Hereditary Autoinflammatory Diseases; Humans; Injections Subcutaneous; Interleukin-1beta; Male; Mevalonate Kinase Deficiency; Young Adult; Medicine (all)030203 arthritis & rheumatologyDose-Response Relationship Drugbusiness.industryHereditary Autoinflammatory DiseasesHyperimmunoglobulinemia Dmedicine.diseaseCanakinumab030104 developmental biologyImmunologyMevalonate Kinase Deficiencybusiness
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Anti-tumour necrosis factor-α antibodies and B cell homeostasis in human inflammatory bowel diseases

2017

Background The expression of CD70 on T cells is greatly enhanced by antigen-presenting cell (APC)-associated signals, such as tumour necrosis factor(TNF)-α, which is constitutionally high in patients with inflammatory bowel disease (IBD). Experimentally, the chronic activation of CD27 as a result of the constitutive expression of CD70 leads to the demise of B cells in bone marrow (BM) and the secondary lymphoid organs. The aim of this study was to assess the number and phenotype of circulating B cell in untreated IBD patients and their counterparts treated with biological anti-TNF drugs. Methods The study involved 13 untreated IBD patients, 36 IBD patients treated with biological drugs, and…

Male0301 basic medicineT-LymphocytesImmunophenotypingB cell homeostasisBiological drugs; Inflammatory bowel diseases; Plasmablasts; TNF-αHomeostasisImmunology and AllergyCD20B-LymphocytesbiologyB-LymphocyteAntibodies MonoclonalMiddle AgedFlow Cytometrymedicine.anatomical_structureFemaleTumor necrosis factor alphaImmunotherapyAntibodyPlasmablastsHumanAdultAdolescentBiological drugImmunologyB-Lymphocyte SubsetsPlasmablastCD19ImmunophenotypingYoung Adult03 medical and health sciencesHomeostasimedicineHumansBiological drugsB cellB-Lymphocyte SubsetPharmacologyTumor Necrosis Factor-alphabusiness.industryInflammatory Bowel DiseaseInflammatory Bowel Diseases030104 developmental biologyT-LymphocyteTNF-αImmunologybiology.proteinBone marrowbusinessCD27 LigandInternational Immunopharmacology
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Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice

2016

Acute pancreatitis (AP) is a common and devastating gastrointestinal disorder that causes significant morbidity. The disease starts as local inflammation in the pancreas that may progress to systemic inflammation and complications. Protein tyrosine phosphatase 1B (PTP1B) is implicated in inflammatory signaling, but its significance in AP remains unclear. To investigate whether PTP1B may have a role in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the effects of pancreatic PTP1B deficiency on cerulein- and arginine-induced acute pancreatitis. We report that PTP1B protein expression was increased in the early phase of AP in mice and rats. In addition, histological an…

Male0301 basic medicineWistarSystemic inflammationMedical and Health SciencesOral and gastrointestinalMicePathology2.1 Biological and endogenous factorsAetiologyNon-Receptor Type 1CancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 1Pancreatitis Acute NecrotizingReverse Transcriptase Polymerase Chain ReactionRegular Articlemedicine.anatomical_structureAcute NecrotizingGastrointestinal disorderAcute pancreatitisTumor necrosis factor alphamedicine.symptomPancreashormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyKnockoutInflammationPathology and Forensic MedicineProinflammatory cytokinePancreatic Cancer03 medical and health sciencesRare DiseasesInternal medicinemedicineAnimalsRats WistarAnimalbusiness.industrymedicine.diseaseRatsDisease Models Animal030104 developmental biologyEndocrinologyPancreatitisDisease ModelsPancreatitisProtein Tyrosine PhosphataseDigestive DiseasesbusinessThe American Journal of Pathology
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Polymorphisms of Pro-Inflammatory IL-6 and IL-1β Cytokines in Ascending Aortic Aneurysms as Genetic Modifiers and Predictive and Prognostic Biomarkers

2021

Background: Previous studies have demonstrated that polymorphisms involved in immune genes can affect the risk, pathogenesis, and outcome of thoracic ascending aortic aneurysms (TAAA). Here, we explored the potential associations of five functional promoter polymorphisms in interleukin-6 (IL-6), IL-1B, IL-1A, IL-18, and Tumor necrosis factor (TNF)A genes with TAAA. Methods: 144 TAAA patients and 150 age/gender matched controls were typed using KASPar assays. Effects on telomere length and levels of TAAA related histopathological and serological markers were analyzed. Results: Significant associations with TAAA risk were obtained for IL-6 rs1800795G&gt

Male0301 basic medicinemedicine.medical_specialtyInterleukin-1betamedial cell apoptosisSingle-nucleotide polymorphism030204 cardiovascular system & hematologyrs16944MicrobiologyPolymorphism Single NucleotideBiochemistryGastroenterologyArticleProinflammatory cytokinePathogenesis03 medical and health sciences0302 clinical medicineAneurysmInternal medicineGenotypeelastic fragmentationmedicinetelomere lengthHumansInterleukin 6thoracic ascending aortic aneurysmsMolecular BiologyAgedAortic Aneurysm ThoracicbiologyInterleukin-6business.industryMMP9Prognosismedicine.diseasers1800795QR1-502Settore MED/23030104 developmental biologyproinflammatory cytokinescystic medial changesbiology.proteinCytokinesBiomarker (medicine)FemaleTumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersBiomolecules
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