Search results for " CYTOKINE"

showing 10 items of 602 documents

Mast cells boost myeloid-derived suppressor cell activity and contribute to the development of tumor-favoring microenvironment

2014

Abstract Inflammation plays crucial roles at different stages of tumor development and may lead to the failure of immune surveillance and immunotherapy. Myeloid-derived suppressor cells (MDSC) are one of the major components of the immune-suppressive network that favors tumor growth, and their interaction with mast cells is emerging as critical for the outcome of the tumor-associated immune response. Herein, we showed the occurrence of cell-to-cell interactions between MDSCs and mast cells in the mucosa of patients with colon carcinoma and in the colon and spleen of tumor-bearing mice. Furthermore, we demonstrated that the CT-26 colon cancer cells induced the accumulation of CD11b+Gr1+ imma…

Cancer Researchmedicine.medical_treatmentCD40 LigandImmunologyInflammationCell CommunicationBiologyNitric OxideProinflammatory cytokineInterferon-gammaMiceImmune systemAntigens CD40Animals; Antigens CD40; CD40 Ligand; Cell Line Tumor; Colonic Neoplasms; Humans; Inflammation; Interferon-gamma; Mast Cells; Mice; Mice Inbred BALB C; Mice Knockout; Myeloid Cells; Nitric Oxide; Tumor Microenvironment; Cell Communication; Cancer Research; Immunology; Medicine (all)Cell Line TumormedicineMast cell; Myeloid-Derived Suppressor Cell; tumor microenvironment; colon cancerTumor MicroenvironmentAnimalsHumansMyeloid-Derived Suppressor CellMast CellMyeloid CellsMast CellsCD40 AntigensMyeloid CellInflammationMice KnockoutTumor microenvironmentColonic NeoplasmMice Inbred BALB CCD40AnimalMedicine (all)ImmunotherapyMast cellmedicine.anatomical_structurecolon cancerImmunologyColonic NeoplasmsCancer researchMyeloid-derived Suppressor Cellbiology.proteinmedicine.symptomHuman
researchProduct

Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
researchProduct

Neuroinflammatory mechanisms in ischemic stroke: Focus on cardioembolic stroke, background, and therapeutic approaches

2020

One of the most important causes of neurological morbidity and mortality in the world is ischemic stroke. It can be a result of multiple events such as embolism with a cardiac origin, occlusion of small vessels in the brain, and atherosclerosis affecting the cerebral circulation. Increasing evidence shows the intricate function played by the immune system in the pathophysiological variations that take place after cerebral ischemic injury. Following the ischemic cerebral harm, we can observe consequent neuroinflammation that causes additional damage provoking the death of the cells; on the other hand, it also plays a beneficial role in stimulating remedial action. Immune mediators are the or…

Cardiac embolismNeuroimmunomodulationIschemiaInflammationReview030204 cardiovascular system & hematologyBioinformaticsCatalysisProinflammatory cytokineBrain IschemiaInorganic Chemistrylcsh:Chemistry03 medical and health sciencesCerebral circulation0302 clinical medicineImmune systemNeuroinflammationmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyNeuroinflammationInflammationEmbolic StrokeIschemic strokebusiness.industryOrganic ChemistryBrainGeneral Medicinemedicine.diseasePathophysiologyComputer Science ApplicationsStrokeEmbolismlcsh:Biology (General)lcsh:QD1-999Cytokinesmedicine.symptombusiness030217 neurology & neurosurgery
researchProduct

Analysis of TCR Vbeta repertoire and cytokine gene expression in patients with idiopathic dilated cardiomyopathy

2001

Although the etiopathogenesis of idiopathic dilated cardiomyopathy (IDC) is still unclear, it is widely accepted that a complex interplay between viral infections and immune mechanisms is the basis of disease genesis. Previously, we showed that heart-infiltrating T cells of patients suffering from acute, fulminant Coxsackie virus B3+-IDC shared a preferential usage of three variable gene segments of the T cell receptor beta chain-(TCR-Vbeta) encoding families Vbeta3, 7 and 13.1. This indicated the possible presence of a superantigen-driven immune response. Here, we further investigated the IDC immunological scenario by analysing different phenotypes of heart-infiltrating cells: TCR repertoi…

Cardiomyopathy DilatedInterleukin 2MyocarditisCD8 AntigensReceptors Antigen T-Cell alpha-betaT cellImmunologyCardiomyopathyGene Expressionchemical and pharmacologic phenomenaPicornaviridaeBiologyHLA-DQ alpha-ChainsImmunoenzyme TechniquesInterferon-gammaImmune systemAntigenHLA-DQ AntigensIdiopathic dilated cardiomyopathymedicineHLA-DQ beta-ChainsHumansImmunology and AllergyRNA MessengerAntigens ViralInterleukin-6Reverse Transcriptase Polymerase Chain ReactionHistocompatibility TestingMyocardiumIDC cytokines immune mechanismsmedicine.diseaseEnterovirus B HumanMyocarditismedicine.anatomical_structureCD4 AntigensImmunologyLeukocytes MononuclearCytokinesInterleukin-2Interleukin-4CD8Interleukin-1medicine.drug
researchProduct

C1-esterase inhibitor in ischemia and reperfusion.

2002

Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…

Cardiotonic AgentsImmunologyIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryPharmacologyComplement C1 Inactivator ProteinsProinflammatory cytokineClassical complement pathwayIschemiamedicineImmunology and AllergyAnimalsHumansAnaphylatoxinComplement Pathway ClassicalCardioprotectionbusiness.industryHeartHematologymedicine.diseaseC1 esteraseComplement systemAnesthesiaModels AnimalbusinessPerfusionComplement C1 Inhibitor ProteinImmunobiology
researchProduct

Altered expression of inflammation-related genes in human carotid atherosclerotic plaques.

2011

Abstract Objective Inflammation is a pivotal process in atherosclerosis development and progression, but the underlying molecular mechanisms remain largely obscure. We have conducted an extensive expression study of atherosclerotic plaques to identify the inflammatory pathways involved in atherosclerosis. Methods We studied 11 human carotid plaques, their respective adjacent regions and 7 control arteries from different subjects. Expression of 92 genes was studied by TaqMan low-density array human inflammation panel. Human aortic endothelial and smooth muscle cells were used for in vitro experiments. Results The mRNA levels of 44/92 genes (48%) differed significantly between the tissues exa…

Carotid Artery DiseasesMalemedicine.medical_specialtyMyocytes Smooth MuscleReceptors ProstaglandinPTGS1InflammationReceptors EpoprostenolSettore MED/22 - Chirurgia VascolareMuscle Smooth VascularCytochrome P-450 Enzyme SystemInternal medicineGene expressionmedicineHumansRNA MessengerReceptors CytokineCells CulturedAgedRegulation of gene expressionInflammationbiologyTumor Necrosis Factor-alphaGene Expression ProfilingMacrophagesEndothelial CellsMiddle AgedCoculture TechniquesPlaque AtheroscleroticGene expression profilingLipoproteins LDLEndocrinologyEicosanoidEicosanoid pathwayGene Expression RegulationItalyAtherosclerosiCase-Control StudiesArachidonate 5-lipoxygenasebiology.proteinCancer researchOxidative streTumor necrosis factor alphaFemaleGene expressionmedicine.symptomInflammation MediatorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesAtherosclerosis
researchProduct

Assessment of alterations in barrier functionality and induction of proinflammatory and cytotoxic effects after sulfur mustard exposure of an in vitr…

2007

Acute lung injury after sulfur mustard (SM) inhalation is characterized by massive, localized hemorrhage and alveolar edema, which implies severe disruption of the vascular and distal airway barrier. In this study, we tested a recently established in vitro coculture model of the alveolo-capillary barrier for its applicability to investigate acute toxic effects of SM at the human respiratory unit. The epithelial compartment of cocultures was exposed to varying concentrations of SM (0-1000 microM; t = 30 min). Following exposure, functional and structural barrier integrity of cocultures was monitored over a period of 24 h. A 50% reduction of transbilayer electrical resistance (TER) within 12-…

Cell SurvivalHealth Toxicology and MutagenesisDNA FragmentationBiologyLung injuryToxicologyProinflammatory cytokinechemistry.chemical_compoundIn vivoCell Line TumorMustard GasHumansTUNEL assayBlood-Air BarrierInterleukinSulfur mustardMolecular biologyCoculture TechniquesCapillariesPulmonary AlveolichemistryCell cultureImmunologyLiberationChemokinesInflammation MediatorsInhalation toxicology
researchProduct

Long-chain fatty alcohols from pomace olive oil modulate the release of proinflammatory mediators

2009

Pomace olive oil is a by-product of olive oil extraction that is traditionally produced and consumed in Spain. The nonglyceride matter of this oil is a good source of interesting minor compounds, like long-chain fatty alcohols, which are present free or as part of waxes. In the present study, long-chain fatty alcohols were isolated from the nonglyceride fraction of pomace olive oil, and the composition was identified and quantified. The major components of long-chain fatty alcohols were tetracosanol, hexacosanol and octacosanol. We investigated the ability of long-chain fatty alcohols from pomace olive oil to inhibit the release of different proinflammatory mediators in vitro by cells invol…

Cell SurvivalNeutrophilsEndocrinology Diabetes and MetabolismClinical BiochemistryNitric Oxide Synthase Type IIBiochemistryProinflammatory cytokineMiceAnimalsPlant OilsPomace olive oilPhospholipases A2 SecretoryMolecular BiologyOlive OilCytokineCalcimycinInflammationNutrition and DieteticsChemistryMacrophagesPomaceNitric oxideRatsThromboxane B2BiochemistryLong-chain fatty alcoholsFatty AlcoholsInflammation MediatorsLong chainOlive oil
researchProduct

Extracellular Vesicles from Neural Stem Cells Transfer IFN-γ via Ifngr1 to Activate Stat1 Signaling in Target Cells

2014

The idea that stem cell therapies work only via cell replacement is challenged by the observation of consistent intercellular molecule exchange between the graft and the host. Here we defined a mechanism of cellular signaling by which neural stem/precursor cells (NPCs) communicate with the microenvironment via extracellular vesicles (EVs), and we elucidated its molecular signature and function. We observed cytokine-regulated pathways that sort proteins and mRNAs into EVs. We described induction of interferon gamma (IFN-γ) pathway in NPCs exposed to proinflammatory cytokines that is mirrored in EVs. We showed that IFN-γ bound to EVs through Ifngr1 activates Stat1 in target cells. Finally, we…

Cell signalingCell CommunicationBiologyArticle3T3 cellsProinflammatory cytokineInterferon-gammaMiceTh2 CellsNeural Stem CellsPrecursor cellmedicineAnimalsInterferon gammaRNA MessengerTransport VesiclesMolecular BiologyReceptors InterferonInflammationBiological Transport3T3 CellsCell BiologyTh1 CellsNeural stem cellCell biologySTAT1 Transcription Factormedicine.anatomical_structureCellular MicroenvironmentSignal transductionStem cellSignal Transductionmedicine.drugMolecular Cell
researchProduct

2013

In multiple sclerosis (MS) autoaggressive T effector cells (Teff) are not efficiently controlled by regulatory T cells (Treg) but the underlying mechanisms are incompletely understood. Proinflammatory cytokines are key factors facilitating Teff activity in chronic inflammation. Here we investigated the influence of IL-6 on Treg sensitivity of Teff from therapy-naive MS patients with or without active disease. Compared to healthy volunteers and independent of disease course CD4+ and especially CD8+ MS-Teff were insensitive against functional active Treg from healthy controls. This unresponsiveness was caused by accelerated production of IL-6, elevated IL-6 receptor expression and phosphoryla…

Cell signalingMultidisciplinarybusiness.industryReceptor expressionProinflammatory cytokineCell biologyImmune systemImmunologyMedicineCytotoxic T cellPhosphorylationbusinessProtein kinase BCD8PLOS ONE
researchProduct