Search results for "Tumor necrosis factor-alpha"

showing 10 items of 504 documents

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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Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion.

2003

The aim of the study was to investigate mitochondrial electron transfer during rat liver reperfusion after cold storage and hypothermic machine perfusion. Livers from male Brown Norway rats were preserved (UW) for 10h either by cold storage (CS) or by hypothermic oxygenated perfusion extracorporal (HOPE). Transhepatic photometric analysis allowed determination of the redox status of mitochondrial cytochromes during preservation, rewarming and reperfusion. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and cyanide in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of …

AnionsMaleTime FactorsCytochromeLightCold storageCaspase 3ElectronsDNA FragmentationMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundSuperoxidesAnimalsCaspase-9CryopreservationCyanidesbiologySuperoxideCaspase 3Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesTemperatureNADH DehydrogenaseGeneral MedicineRotenoneDNAOrgan PreservationLipid MetabolismCaspase 9MitochondriaRatsCold TemperatureOxygenLight intensitychemistryBiochemistryElectron Transport Chain Complex ProteinsLiverCaspasesReperfusionbiology.proteinCytochromesLipid PeroxidationMitogen-Activated Protein KinasesGeneral Agricultural and Biological SciencesReactive Oxygen SpeciesOxidation-ReductionCryobiology
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Mitochondrial glutathione depletion by glutamine in growing tumor cells.

2000

The effect of L-glutamine (Gln) on mitochondrial glutathione (mtGSH) levels in tumor cells was studied in vivo in Ehrlich ascites tumor (EAT)-bearing mice. Tumor growth was similar in mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln) or a nutritionally complete elemental diet (SD). As compared with non-tumor-bearing mice, tumor growth caused a decrease of blood Gln levels in mice fed an SD but not in those fed a GED. Tumor cells in mice fed a GED showed higher glutaminase and lower Gln synthetase activities than did cells isolated from mice fed an SD. Cytosolic glutamate concentration was 2-fold higher in tumor cells from mice fed a GED ( approximately…

AnionsMalemedicine.medical_specialtyFree RadicalsGlutamineOxidative phosphorylationBiologyMitochondrionMitochondrial Sizemedicine.disease_causeBiochemistryGlutaminase activitychemistry.chemical_compoundMiceAdenosine TriphosphatePhysiology (medical)Internal medicinemedicineAnimalsHumansAmino AcidsCarcinoma Ehrlich TumorGlutaminaseTumor Necrosis Factor-alphaGlutathioneHydrogen-Ion ConcentrationGlutathioneRecombinant ProteinsMitochondriaGlutamineOxidative StressEndocrinologyBiochemistrychemistryOxidative stressFree radical biologymedicine
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Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis

2017

Objective: To investigate the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of ankylosing spondylitis (AS). Methods: Patients who met the modified New York criteria for AS were recruited for the study. Healthy volunteers, rheumatoid arthritis patients, and osteoarthritis patients were included as controls. Based on the annual rate of increase in modified Stoke AS Spine Score (mSASSS), AS patients were classified as progressors or nonprogressors. MIF levels in serum and synovial fluid were quantitated by enzyme-linked immunosorbent assay. Predictors of AS progression were evaluated using logistic regression analysis. Immunohistochemical analysis of ileal tissue was…

AnkylosingAdultMaleLogistic ModelMacrophageImmunologyEnzyme-Linked Immunosorbent AssayIntramolecular OxidoreductasePredictive Value of TestMonocyteSeverity of Illness IndexCalcificationCalcification PhysiologicPaneth CellRheumatologySynovial Fluidotorhinolaryngologic diseasesImmunology and AllergySpondylitis AnkylosingPhysiologicSpondylitiMacrophage Migration-Inhibitory FactorTumor Necrosis Factor-alphaOsteoblastB-LymphocyteHistocompatibility Antigens Class IIMiddle AgedSpineAntigens Differentiation B-LymphocyteSettore MED/16 - ReumatologiaAntigenDifferentiationDisease ProgressionFemaleCase-Control StudieHuman
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Identification of epitopes of Mycobacterium tuberculosis 16-kDa protein recognized by human leukocyte antigen-A*0201 CD8(+) T lymphocytes.

2002

CD8(+) T cells could make an important contribution to protection against tuberculosis (TB), but the antigenic determinants recognized in the context of major histocompatibility complex class I molecules remain ill defined. Our aim was to identify nonamer peptides derived from the acr/16-kDa antigen. Two immunogenic peptides (p21-29 and p120-128) were identified by their ability to elicit cytotoxic CD8(+) T cells from juvenile patients recovering from TB. Epitope-specific recognition was demonstrated by the lysis of both Mycobacterium tuberculosis-infected and peptide-pulsed macrophages, the release of cytotoxic granules, and interferon-gamma and tumor necrosis factor-alpha production. CD8(…

Antigens Differentiation T-LymphocyteCytotoxicity ImmunologicMalePore Forming Cytotoxic ProteinsT cellEpitopes T-LymphocyteHuman leukocyte antigenCD8-Positive T-LymphocytesMajor histocompatibility complexEpitopeInterferon-gammaImmune systemAntigenBacterial ProteinsHLA-A2 AntigenmedicineImmunology and AllergyCytotoxic T cellHumansChildTuberculosis PulmonaryMembrane GlycoproteinsbiologyHLA-A AntigensPerforinTumor Necrosis Factor-alphaMacrophagesMycobacterium tuberculosisFlow CytometryPeptide FragmentsMolecular WeightInfectious Diseasesmedicine.anatomical_structureImmunologybiology.proteinFemaleCD8The Journal of infectious diseases
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Peritoneal Cavity is a Route for Gut-Derived Microbial Signals to Promote Autoimmunity in Non-Obese Diabetic Mice

2015

Macrophages play a crucial role in innate immune reactions, and peritoneal macrophages (PMs) guard the sterility of this compartment mainly against microbial threat from the gut. Type 1 diabetes (T1D) is an autoimmune disease in which gut microbiota and gut immune system appear to contribute to disease pathogenesis. We have recently reported elevated free radical production and increased permeability of gut epithelium in non-obese diabetic (NOD) mice. Impaired barrier function could lead to bacterial leakage to the peritoneal cavity. To explore the consequences of impaired gut barrier function on extra-intestinal immune regulation, we characterized peritoneal lavage cells from young newly w…

Antigens Differentiation T-LymphocyteLipopolysaccharidesmedicine.medical_specialtymiceT-LymphocytesT cellBlotting WesternImmunologyWeaningNodBiologyta3111Peritoneal cavityImmune systemSpecies SpecificityAntigens CDMice Inbred NODInternal medicinediabeticmedicineAnimalsLectins C-TypeIntestinal Mucosamicrobial signalsCells CulturedNOD miceMice Inbred BALB CInnate immune systemTumor Necrosis Factor-alphanon-obeseMicrobiotaautoimmunityta1182ta3141General MedicineFlow CytometryGut EpitheliumIntestinesMice Inbred C57BLInterleukin-1 Receptor-Associated KinasesEndocrinologymedicine.anatomical_structureperitoneal cavityImmunologyMacrophages PeritonealTumor necrosis factor alphaInjections IntraperitonealSignal TransductionScandinavian Journal of Immunology
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Inducible Co-Stimulator Null MRL-Fas lpr Mice

2005

MRL/MpJ-Tnfrsf6lpr (MRL-Faslpr) mice develop a spontaneous T cell-dependent autoimmune disease that shares features with human lupus, including fatal nephritis, systemic pathology, and autoantibodies (autoAb). The inducible co-stimulator (ICOS) is upregulated on activated T cells and modulates T cell-mediated responses. To investigate whether ICOS has an essential role in regulating autoimmune lupus nephritis and the systemic illness in MRL-Faslpr mice, ICOS null (-/-) MRL Faslpr and ICOS intact (+/+) MRL-Faslpr strains (wild-type [WT]) were generated and compared. It was determined that in ICOS-/- MRL-Faslpr as compared with the WT strain, (1) there is a significant reduction in circulatin…

Antigens Differentiation T-LymphocyteMice Inbred MRL lprT-LymphocytesT cellLupus nephritismedicine.disease_causeBlood Urea NitrogenAutoimmunityInducible T-Cell Co-Stimulator ProteinInterferon-gammaMiceImmune systemimmune system diseasesmedicineAnimalsskin and connective tissue diseasesAutoantibodiesMice Inbred C3HSystemic lupus erythematosusTumor Necrosis Factor-alphabusiness.industryAutoantibodyGeneral Medicinemedicine.diseaseLupus NephritisIsotypeInterleukin-10Mice Inbred C57BLProteinuriamedicine.anatomical_structureNephrologyImmunoglobulin GImmunologyInterleukin-4businessNephritisJournal of the American Society of Nephrology
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Synthesis and evaluation of diverse thio avarol derivatives as potential UVB photoprotective candidates.

2007

Semisynthesis of 13 new thio avarol derivatives (4-16) and in vitro evaluation on the photodamage response induced by UVB irradiation are described. Their ability to inhibit NF-kappaB activation and TNF-alpha generation in HaCaT cells as well as their antioxidant capacity in human neutrophils has also been studied. Among them we have identified two monophenyl thio avarol derivatives (4-5) lacking cytotoxicity which can be considered promising UVB photoprotective agents through the potent inhibition of NF-kappaB activation with a mild antioxidant pharmacological profile.

AntioxidantMagnetic Resonance SpectroscopyNeutrophilsPhotochemistryUltraviolet Raysmedicine.medical_treatmentChemistry PharmaceuticalClinical BiochemistryMolecular ConformationPharmaceutical ScienceThio-BiochemistryChemical synthesisAntioxidantsCell Line TumorDrug DiscoverymedicineHumansCytotoxicityMolecular Biologyintegumentary systemChemistryTumor Necrosis Factor-alphaOrganic ChemistryNF-kappa BSemisynthesisIn vitroHaCaTmedicine.anatomical_structureBiochemistryModels ChemicalDrug DesignMolecular MedicineKeratinocyteReactive Oxygen SpeciesSesquiterpenesBioorganicmedicinal chemistry letters
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Tumor necrosis factor alpha polymorphism C-850T is not associated with Alzheimer's disease and vascular dementia in an Italian population.

2003

A pathogenic role of inflammatory factors has been proposed both in Alzheimer's disease (AD) and vascular dementia (VD). A previous report indicated the presence of polymorphism C-850T of tumor necrosis factor (TNF) alpha as a genetic risk factor for VD and, associated with apolipoprotein E epsilon 4, for AD. We have assessed the association between TNF-alpha polymorphism and dementias in Italian populations of AD, VD and elderly controls. The influence of TNF-alpha polymorphism on dementia has not been confirmed in this segment of the Italian population.

Apolipoprotein EMalePathologymedicine.medical_specialtyGenotypemedicine.medical_treatmentCentral nervous system diseaseDegenerative diseaseAlzheimer DiseaseRisk FactorsmedicineDementiaHumansVascular dementiaAgedAged 80 and overPolymorphism Geneticbusiness.industryTumor Necrosis Factor-alphaGeneral Neurosciencemedicine.diseaseCytokineItalyImmunologyTumor necrosis factor alphaDementiaFemaleAlzheimer's diseasebusinessNeuroscience letters
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Induction of annexin-1 during TRAIL-induced apoptosis in thyroid carcinoma cells

2005

We investigated the expression of annexin-1 (ANXA1) in thyroid carcinoma cell lines and in thyroid cancers with a different degree of differentiation. The highest level of ANXA1 expression examined by Western blotting was detected in the papillary carcinoma cells (NPA) and in the follicular cells (WRO). On the other hand, the most undifferentiated thyroid carcinoma cells (ARO and FRO) presented the lowest level of ANXA1 expression. In surgical tissue specimens from 32 patients with thyroid cancers, we found high immunoreactivity for ANXA1 in papillary (PTC) and follicular (FTC) thyroid cancers while in undifferentiated thyroid cancers (UTC) the expression of the protein was barely detectabl…

ApoptosisTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsthyroidThyroid carcinomaTNF-Related Apoptosis-Inducing LigandText miningAnnexinMedicineHumansThyroid NeoplasmsMolecular BiologyThyroid NeoplasmAnnexin A1Apoptosis Regulatory ProteinMembrane Glycoproteinsbusiness.industryTumor Necrosis Factor-alphaApoptosiCell BiologyApoptosisCancer researchMembrane GlycoproteinbusinessApoptosis Regulatory ProteinsHuman
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