Search results for "TNFR"

showing 10 items of 12 documents

Clinical Features at Onset and Genetic Characterization of Pediatric and Adult Patients with TNF-α Receptor—Associated Periodic Syndrome (TRAPS): A S…

2020

This study explores demographic, clinical, and therapeutic features of tumor necrosis factor receptor-associated periodic syndrome (TRAPS) in a cohort of 80 patients recruited from 19 Italian referral Centers. Patients’ data were collected retrospectively and then analyzed according to age groups (disease onset before or after 16 years) and genotype (high penetrance (HP) and low penetrance (LP) TNFRSF1A gene variants). Pediatric- and adult-onset were reported, respectively, in 44 and 36 patients; HP and LP variants were found, respectively, in 32 and 44 cases. A positive family history for recurrent fever was reported more frequently in the pediatric group than in the adult group (p<0.05…

0301 basic medicinemyalgiaMaleAbdominal painSettore MED/16 - REUMATOLOGIATNFRSF1AGene mutationGastroenterology0302 clinical medicinePathologyMedicineRB1-214PericarditisChildPrognosisPenetranceInflamacióFamilial Mediterranean FeverAIDA networkEstudi de casosReceptors Tumor Necrosis Factor Type IChild PreschoolAutoinflammationFemalemedicine.symptomResearch ArticleAdultmedicine.medical_specialtyArticle SubjectAdolescentGenotypetumor necrosis factorImmunologyContext (language use)Asymptomatic03 medical and health sciencesYoung AdultInternal medicineAnimalsHumansRetrospective Studies030203 arthritis & rheumatologyInflammationbusiness.industrytumor necrosis factor TRAPS AIDA networkTumor Necrosis Factor-alphaInfantTRAPSCell BiologyMyalgiaBiological productmedicine.disease030104 developmental biologyMutationCase studiesbusinessKidney diseaseMediators of Inflammation
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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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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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Intrinsic TNFR2 signaling in T regulatory cells provides protection in CNS autoimmunity

2018

Significance In spite of TNF involvement in the pathogenesis of multiple sclerosis (MS), systemic TNF neutralization in MS patients was not successful. One of the possible reasons is that TNF possesses both pathogenic and protective features that may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one of such protective functions of TNF mediated by intrinsic TNFR2 signaling in Treg cells. In mice bearing humanized TNF and TNFR2 genetic loci, TNFR2 ablation restricted to Treg cells led to reduced capacity to control Th17 cell responses, exacerbated experimental autoimmune encephalomyelitis (EAE) development, and affected the maintenance of Treg cells. These findings…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT regulatory cellsmedicine.medical_treatmentAutoimmunitychemical and pharmacologic phenomenaBiologymedicine.disease_causeT-Lymphocytes RegulatoryneuroinflammationAutoimmunityMice03 medical and health sciencesImmunology and Inflammation0302 clinical medicineImmune systemmedicineAnimalsHumansReceptors Tumor Necrosis Factor Type IIIL-2 receptorCells CulturedNeuroinflammationMice KnockoutAutoimmune diseaseMultidisciplinaryEAETumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisFOXP3hemic and immune systemsBiological Sciencesmedicine.diseaseTNF/TNFR2Mice Inbred C57BLDisease Models Animalhumanized mice030104 developmental biologyCytokineGene Expression RegulationImmunology030215 immunologyProceedings of the National Academy of Sciences
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SARS CoV2 infection _The longevity study perspectives

2021

Graphical abstract

MaleAgingssRNA single-stranded RNARFLP restriction fragment length polymorphismHSPs heat shock proteinsReviewPTMs post-translational modificationsSevere Acute Respiratory SyndromeBiochemistryHIV-1 human immunodeficiency virus-1TNF-α tumor necrosis factor-αEC endothelial cells0302 clinical medicineFluAV influenza A virusI insertionMedicineIFN-γ interferon-γDIC disseminated intravascular coagulationPCR Polymerase Chain Reactionmedia_commonAged 80 and overLongevityRBD receptor-binding domainNeurologyLongevity modelMI myocardial infarctionNK natural killerhPIV2 human parainfluenza virus type 2media_common.quotation_subjectResearching genetic basis of resistance and potential pharmacological targetsLongevityDBP diastolic blood pressureNF-Kb nuclear transcription factor kBRANTES regulated upon activation normal T cell expressed and secretedMphi human macrophages03 medical and health sciencesCox 2 cyclooxygenase 2ORF open reading framePT prothrombin timeSettore MED/05 - Patologia ClinicaHumansMolecular BiologyInflammatory genesARDS acute respiratory distress syndromeNO nitric oxideD deletionCpGIs CpG islandsT2DM type 2 diabetes mellitusmedicine.diseaseFDP fibrin degradation products030104 developmental biologySARS CoV2 severe acute respiratory syndrome Coronavirus 2 virusImmunologyBMI body max indexItalian nonagenarians/centenariansRSV respiratory syncytial virusComplication030217 neurology & neurosurgeryMAPK mitogen-activated protein kinaseIP-10 IFN-γ -Inducible Protein 1040301 basic medicineAT1R activity of angiotensin 1 receptorsDCs dentritic cellsSSCP single strand conformation polymorphismACE/DD polymorphism of the angiotensin converting enzymeFGF21 fibroblast growth factor 21TLR4 toll-like receptor 4NAD nicotinamide adenine dinucleotideACE angiotensin-I converting enzymeAT2R activity of angiotensin 2 receptorsCOVID-19 Coronavirus disease 2019Respiratory distressACE2 angiotensin converting enzyme 2MKP-1 mitogen-activated protein kinase phosphatase-1 ()PD protease domainSNP single nucleotide polymorphismEH essential hypertensionTNFR tumor necrosis factor receptorINR international normalized ratio of the prothrombin timePAI-1 plasminogen activator inhibitor-1Ang angiotensinLPS lipopolysaccharideMCP1 monocyte chemoattractant protein-1medicine.symptomaPTT partial thromboplastin timeBiotechnologyDUSP1 dual specificity phosphatase 1Coronavirus disease 2019 (COVID-19)PC prostate cancerRAS renin-angiotensin aldosterone systemCCR5Δ32 genetic variant of chemokine receptorCOVID-19 Researching genetic basis of resistance and potential pharmacological targets Italian nonagenarians/centenarians Longevity modelAsymptomaticSARS-1 severe acute respiratory syndrome virus 1SIRT-1 Sirtuin 1Th1 t-helper lymphocyte type 1Immune systemROS reactive oxygen speciesTGF-β transforming growth factor betaET-1 endothelin-1ComputingMethodologies_COMPUTERGRAPHICSADAM-17 metallopeptidase domain 17business.industrySARS-CoV-2SBP systolic blood pressureCOVID-19HDACs histone deacetylasesComorbidityImmune Systembusiness5-LO lipoxygenase 5Ageing Research Reviews
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Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats.

2020

Minimal hepatic encephalopathy is associated with changes in the peripheral immune system which are transferred to the brain, leading to neuroinflammation and thus to cognitive and motor impairment. Mechanisms by which changes in the immune system induce cerebral alterations remain unclear. Extracellular vesicles (EVs) seem to play a role in this process in certain pathologies. The aim of this work was to assess whether EVs play a role in the induction of neuroinflammation in cerebellum and motor incoordination by chronic hyperammonemia. We characterized the differences in protein cargo of EVs from plasma of hyperammonemic and control rats by proteomics and Western blot. We assessed whether…

MaleCerebellumtnfαhepatic encephalopathyArticleExtracellular VesiclesImmune systemWestern blotmedicineAnimalsHumansHyperammonemiaRats WistarReceptorlcsh:QH301-705.5NeuroinflammationInflammationMicrogliamedicine.diagnostic_testbusiness.industryTumor Necrosis Factor-alphaHyperammonemiaGeneral Medicinetnfα receptor tnfr1medicine.diseaseRatsMotor Skills DisordersDisease Models Animalmedicine.anatomical_structurelcsh:Biology (General)glial activationTumor necrosis factor alphaNervous System DiseasesTNF alpha receptor TNFR1businessNeuroscienceTNF alpha
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Increased immunosuppressive function of CD4(+)CD25(+)Foxp3(+)GITR+ T regulatory cells from NFATc2((-/-)) mice controls allergen-induced experimental …

2012

The expansion of effector T cells is tightly controlled by transcription factors like nuclear factor of activated T cells (NFAT) family members that mediate early intracellular responses to T cell receptor-mediated signals. In this study we show that, after allergen challenge, NFATc2((-/-)) mice had augmented number of functionally intact CD4(+)CD25(++)GITR(++) T regulatory (T regs) cells in the lung. Anti-GITR antibody treatment inhibited T regulatory cell function and enhanced the number of activated lung CD4(+) T cells associated with increased IL-2 and pSTAT-5 in the airways of NFATc2((-/-)) mice in experimental allergic asthma. This agonistic treatment led to increased inflammation in …

NFATC2T cellImmunologyInflammationBiologyT-Lymphocytes RegulatoryInterleukin 21MiceTh2 CellsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyAnimalsIL-2 receptorLungImmunosuppression TherapyMice KnockoutNFATC Transcription FactorsInterleukin-2 Receptor alpha SubunitFOXP3NFATForkhead Transcription FactorsHematologyAllergensAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinCytokinesTh17 CellsFemalemedicine.symptomAntibodySpleenImmunobiology
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress.

2012

Cells are constantly exposed to endogenous and exogenous cellular injuries. They cope with stressful stimuli by adapting their metabolism and activating various “guardian molecules.” These pro-survival factors protect essential cell constituents, prevent cell death, and possibly repair cellular damages. The Inhibitor of Apoptosis (IAPs) proteins display both anti-apoptotic and pro-survival properties and their expression can be induced by a variety of cellular stress such as hypoxia, endoplasmic reticular stress and DNA damage. Thus, IAPs can confer tolerance to cellular stress. This review presents the anti-apoptotic and survival functions of IAPs and their role in the adaptive response to…

Programmed cell deathDNA damageCellCellular homeostasisReviewUPRInhibitor of apoptosisDNA damage responseNF-κBneurodegenerative diseaseMedicinecancerNF-kBlcsh:QH301-705.5Caspasebiologybusiness.industryEndoplasmic reticulumapoptosisGeneral MedicineCell biologyIAPsmedicine.anatomical_structurelcsh:Biology (General)caspasesApoptosisImmunologyTNFRbiology.proteinbusinessCells
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