Search results for " Tumor necrosis factor"

showing 10 items of 110 documents

Induction of the cytokine TWEAK and its receptor Fn14 in ischemic stroke.

2008

Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels o…

AdultMalemedicine.medical_treatmentEnzyme-Linked Immunosorbent AssayFunctional LateralityReceptors Tumor Necrosis FactorCerebral edemaBrain ischemiaCell surface receptorMedicineHumanscardiovascular diseasesRNA MessengerReceptorStrokeCytokine TWEAKAgedAged 80 and overbusiness.industryCerebral infarctionBrainCytokine TWEAKMiddle Agedmedicine.diseaseUp-RegulationStrokeCytokineNeurologyTWEAK ReceptorCase-Control StudiesImmunologyTumor Necrosis FactorsFemaleNeurology (clinical)businessJournal of the neurological sciences
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Safety of etanercept therapy in rheumatoid patients undergoing surgery: preliminary report

2009

This is a preliminary report on a case-series of rheumatoid patients that underwent various kinds of elective surgery but did not withdraw etanercept therapy in spite of physician advise. Elective surgery consisted of right knee surgical prosthesis, bilateral cataract, bilateral hallux valgus, right hip prosthesis, bladder stone by cystoscopy and left inguinal hernia. All the patients had a regular healing rate. During follow-up (6-12 months) no one of these patients were suffering from infective complications after surgery. According to same recent literature results, our data suggest that it is the time to value rheumatoid patient preferences through a correct information about cost-benef…

AdultMalemusculoskeletal diseasesmedicine.medical_specialtySettore MED/09 - Medicina InternaPilot ProjectsReceptors Tumor Necrosis FactorEtanerceptEtanerceptArthritis RheumatoidPostoperative ComplicationsPatient satisfactionRheumatologyInternal medicinemedicineHumansPostoperative PeriodElective surgeryWound Healingmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryContraindicationsGeneral MedicineCystoscopyMiddle Agedmedicine.diseaseRheumatologySurgerySettore MED/16 - ReumatologiaTolerabilityElective Surgical ProceduresImmunoglobulin GRheumatoid arthritisFemaleBiological therapy Decompensated diabetes mellitus Etanercept Polymyalgia rheumatica Steroid therapy.businessAdverse drug reactionmedicine.drugClinical Rheumatology
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Inflammation, genes and zinc in ageing and age-related diseases.

2006

Lifelong antigenic burden determines a condition of chronic inflammation, with increased lymphocyte activation and pro-inflammatory cytokine production. A large number of studies have documented changes in Zn metabolism in experimental animal models of acute and chronic inflammation and in human chronic inflammatory diseases. In particular, modification of zinc plasma concentration as well as intracellular disturbance of antioxidant intracellular pathways have been found associated to age-related inflammatory diseases, like atherosclerosis. Zinc deficiency is extremely diffused in aged people that are educated to avoid meat and other high Zn-content foods due to fear of cholesterol. Rather,…

Agingmedicine.medical_treatmentLongevityGene ExpressionInflammationBiologychemistry.chemical_compoundmedicinecytokine interleukin 6 metallothionein tumor necrosis factor alpha zincAnimalsHumansGeneTranscription factorCellular SenescenceInflammationPolymorphism GeneticCholesterolInterleukin-6Tumor Necrosis Factor-alphamedicine.diseaseAtherosclerosisImmunity InnateZincCytokinechemistryAgeingImmunologyZinc deficiencyCytokinesMetallothioneinGeriatrics and Gerontologymedicine.symptomGerontologyIntracellular
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Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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T cell killing by tolerogenic dendritic cells protects mice from allergy.

2011

It is well established that allergy development can be prevented by repeated low-dose exposure to contact allergens. Exactly which immune mechanisms are responsible for this so-called low zone tolerance (LZT) is not clear, although CD8⁺ suppressor T cells are known to have a role. Here, we show that TNF released by tolerogenic CD11⁺CD8⁺ DCs located in skin-draining lymph nodes is required and sufficient for development of tolerance to contact allergens in mice. DC-derived TNF protected mice from contact allergy by inducing apoptosis in allergen-specific effector CD8⁺ T cells via TNF receptor 2 but did not contribute to the generation and function of the regulatory T cells associated with LZ…

AllergyT cellApoptosisBiologyCD8-Positive T-LymphocytesDermatitis Contactlaw.inventionImmune toleranceMicelawmedicineHypersensitivityImmune ToleranceAnimalsReceptors Tumor Necrosis Factor Type IIReceptorMice KnockoutEffectorTumor Necrosis Factor-alphaGeneral MedicineDendritic CellsAllergensmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologySuppressorTumor necrosis factor alphaThe Journal of clinical investigation
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Obesity and Outcomes in COVID-19: When an Epidemic and Pandemic Collide.

2020

Obesity has reached epidemic proportions in the United States and in much of the westernized world, contributing to considerable morbidity. Several of these obesity-related morbidities are associated with greater risk for death with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 penetrates human cells through direct binding with angiotensin-converting enzyme 2 receptors on the cell surface. Angiotensin-converting enzyme 2 expression in adipose tissue is higher than that in lung tissue, which means that adipose tissue may be vulnerable to COVID-19 infection. Obese patients also have worse outcomes with COVID-19 infection, including respiratory failure, n…

BMI body mass indexmedicine.medical_treatmentAdipose tissue030204 cardiovascular system & hematologyCHD coronary heart diseaseHF heart failureUS United States0302 clinical medicineRAAS renin-angiotensin-aldosterone systemPandemicMedicine030212 general & internal medicineCDC Centers for Disease Control and PreventionCOVID-19 coronavirus disease 2019TNF tumor necrosis factorHFpEF HF with preserved ejection fractionCV cardiovascularGeneral MedicinePrognosisICU intensive care unitPA physical activityMetS metabolic syndromePAH pulmonary arterial hypertensionCoronavirus Infectionsmedicine.medical_specialtyAF atrial fibrillationACE angiotensin-converting enzymePneumonia ViralCVD cardiovascular diseaseSARS-CoV-2 severe acute respiratory syndrome coronavirus 2ArticleSeverity03 medical and health sciencesBetacoronavirusInternal medicineIPF idiopathic pulmonary fibrosisHumansObesityMortalityHTN hypertension or hypertensivePandemicsMechanical ventilationAng II angiotensin IIbusiness.industrySARS-CoV-2CKD chronic kidney diseaseCOVID-19T2DM type 2 diabetes mellitusmedicine.diseaseAngiotensin IIObesityIL interleukinPneumoniaRespiratory failureMetabolic syndromebusinessSNS sympathetic nervousMayo Clinic proceedings
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A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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Regulatory activity of human CD4 CD25 T cells depends on allergen concentration, type of allergen and atopy status of the donor.

2005

Regulatory CD4+ CD25+ FoxP3-positive T cells (Treg) are functional in most atopic patients with allergic rhinitis and are able to inhibit T helper type 1 (Th1) and Th2 cytokine production of CD4+ CD25- T cells. This study was designed to analyse the following additional aspects: influence of allergen concentration, influence of the type of allergen, and influence of the atopy status of the donor on the strength of the regulatory activity. CD4+ CD25- T cells from healthy non-atopic controls or from grass-pollen-allergic or wasp-venom-allergic donors were stimulated alone or in the presence of Treg with autologous mature monocyte-derived dendritic cells which were pulsed with different concen…

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergymedicine.medical_treatmentImmunologyDose-Response Relationship Immunologicchemical and pharmacologic phenomenaWasp VenomsReceptors Nerve Growth FactorBiologymedicine.disease_causePoaceaeReceptors Tumor Necrosis FactorAtopyInterleukin 21AllergenTh2 CellsAntigenT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyHumansIL-2 receptorReceptorCells CulturedCell Proliferationhemic and immune systemsForkhead Transcription FactorsReceptors Interleukin-2Original ArticlesAllergensTh1 Cellsmedicine.diseaseCoculture TechniquesCytokineImmunologyCytokinesPollenImmunology
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Antibodies against tumor necrosis factor (TNF) induce T-cell apoptosis in patients with inflammatory bowel diseases via TNF receptor 2 and intestinal…

2011

Background & Aims The anti–tumor necrosis factor (TNF) antibodies infliximab, adalimumab, and certolizumab pegol have proven clinical efficacy in Crohn's disease. Here, we assessed the effects of anti-TNF antibodies on apoptosis in inflammatory bowel disease (IBD). Methods CD14 + macrophages and CD4 + T cells were isolated from peripheral blood and lamina propria mononuclear cells from patients with IBD and control patients. Cell surface markers and apoptosis were assessed by immunohistology and fluorescence-activated cell sorting techniques. Results Lamina propria CD14 + macrophages showed significantly more frequent and higher membrane-bound TNF (mTNF) expression than CD4 + T cells in IBD…

CD4-Positive T-LymphocytesMaleNecrosisCD14Anti-Inflammatory AgentsLipopolysaccharide ReceptorsApoptosisEnzyme-Linked Immunosorbent AssayBiologyAntibodies Monoclonal HumanizedReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellPolyethylene GlycolsImmunoglobulin Fab FragmentsYoung AdultmedicineHumansReceptors Tumor Necrosis Factor Type IIAntigen-presenting cellAgedLamina propriaHepatologyCluster of differentiationTumor Necrosis Factor-alphaMacrophagesGastroenterologyAdalimumabAntibodies MonoclonalMiddle AgedFlow CytometryInflammatory Bowel DiseasesInfliximabmedicine.anatomical_structureApoptosisCase-Control StudiesImmunologyCertolizumab PegolTumor necrosis factor alphaFemalemedicine.symptomGastroenterology
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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