Search results for " cytokine"

showing 10 items of 602 documents

CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 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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Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulati…

2001

Chronic, nonhealing wounds represent a major clinical challenge to practically all disciplines in modern medicine including dermatology, oncology, surgery, and hematology. In skin wounds, granulocyte-macrophage colony stimulating factor (GM-CSF) is secreted by keratinocytes shortly after injury and mediates epidermal cell proliferation in an autocrine manner. Many other cells involved in wound healing including macrophages, lymphocytes, fibroblasts, endothelial cells, and dendritic cells synthesize GM-CSF and/or are targets of this cytokine. Therefore, GM-CSF is a pleiotropic cytokine evoking complex processes during wound repair. Despite this complexity and the scarcity of mechanistic unde…

Macrophage colony-stimulating factorKeratinocytesMalemedicine.medical_treatmentGene ExpressionMitosisNeovascularization PhysiologicMice TransgenicDermatologytransgenic miceBiologyBiochemistryProinflammatory cytokineTransforming Growth Factor beta1MiceTransforming Growth Factor betamedicineAnimalsRNA MessengerAutocrine signallingMolecular BiologySkinWound Healingintegumentary systemGranulation tissueGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFCell BiologyUp-RegulationCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyModels AnimalCancer researchCarcinogensGranulation TissueCytokinesTetradecanoylphorbol AcetateFemaleKeratinocyteWound healingmedicine.drugJournal of Investigative Dermatology
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Fine-tuning nucleophosmin in macrophage differentiation and activation

2011

Abstract M-CSF–driven differentiation of peripheral blood monocytes is one of the sources of tissue macrophages. In humans and mice, the differentiation process involves the activation of caspases that cleave a limited number of proteins. One of these proteins is nucleophosmin (NPM1), a multifunctional and ubiquitous protein. Here, we show that caspases activated in monocytes exposed to M-CSF cleave NPM1 at D213 to generate a 30-kDa N-terminal fragment. The protein is further cleaved into a 20-kDa fragment, which involves cathepsin B. NPM1 fragments contribute to the limited motility, migration, and phagocytosis capabilities of resting macrophages. Their activation with lipopolysaccharides …

Macrophage colony-stimulating factorLipopolysaccharidesCellular differentiationImmunologyBiochemistryProinflammatory cytokine03 medical and health sciencesPhagocytes Granulocytes and MyelopoiesisMice0302 clinical medicineAnimalsHumansNuclear proteinCaspaseCells Cultured030304 developmental biologyMice Knockout0303 health sciencesNucleophosminbiologyMacrophage Colony-Stimulating FactorMacrophagesNuclear ProteinsCell DifferentiationCell BiologyHematologyMacrophage ActivationNFKB1Molecular biologyCathepsinsCell biologyProtein Structure TertiaryCXCL1Mice Inbred C57BL030220 oncology & carcinogenesisCaspasesbiology.proteinNucleophosminProtein Processing Post-TranslationalBlood
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The Microbiota Promotes Arterial Thrombosis in Low-Density Lipoprotein Receptor-Deficient Mice

2019

Our results demonstrate a functional role for the commensal microbiota in atherothrombosis. In a ferric chloride injury model of the carotid artery, GF C57BL/6J mice had increased occlusion times compared to colonized controls. Interestingly, in late atherosclerosis, HFD-fed GF Ldlr−/− mice had reduced plaque rupture-induced thrombus growth in the carotid artery and diminished ex vivo thrombus formation under arterial flow conditions.

Male0209 industrial biotechnologyVery low-density lipoproteinChemokine CXCL102 engineering and technology030204 cardiovascular system & hematologyarterial thrombosisApplied Microbiology and BiotechnologyACTIVATIONMicechemistry.chemical_compound020901 industrial engineering & automation0302 clinical medicinegermfree0202 electrical engineering electronic engineering information engineeringMedicinevascular inflammationPlateletChemokine CCL7lcsh:QH301-705.5platelet0303 health sciencesatherosclerosis mouse modelsfood and beveragesThrombosisPlaque AtheroscleroticQR1-502late atherosclerosis3. Good healthHolobiontlow-density lipoprotein receptorgerm-freeplateletscardiovascular systemFemalelipids (amino acids peptides and proteins)GLYCOPROTEIN-VIBlood streamResearch ArticleRECRUITMENTmedicine.medical_specialtyNutritional compositionCOAGULATION610 Medicine & healthBiologyMETABOLISMBiochemistry Genetics and Molecular Biology (miscellaneous)MicrobiologyMicrobiologyHost-Microbe BiologyProinflammatory cytokinePLATELET HYPERREACTIVITY03 medical and health sciencesINFLAMMATIONVirologyInternal medicineatherothrombosisGeneticsmicrobiotaAnimalsInterleukin 9Platelet activationcardiovascular diseasesThrombusMolecular Biology030304 developmental biologygut microbiotabusiness.industryCholesterolcarotid artery020208 electrical & electronic engineeringcholesterolnutritional and metabolic diseasesCell Biologymedicine.diseaseMicroreviewCHLAMYDIA-PNEUMONIAEMice Mutant StrainsGastrointestinal MicrobiomeEndocrinologyReceptors LDLlcsh:Biology (General)chemistryArterial thrombusLDL receptorParasitologyatherosclerosisbusinessEx vivoLipoproteinmBio
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Anti-cytokine therapy for prevention of atherosclerosis

2015

Abstract Background Currently a chronic inflammation is considered to be the one of the most important reasons of the atherosclerosis progression. A huge amount of researches over the past few decades are devoted to study the various mechanisms of inflammation in the development of atherosclerotic lesions. Purpose To review current capabilities of anti-inflammatory therapy for the prevention and treatment of atherosclerosis and its clinical manifestations. Methods Appropriate articles on inflammatory cytokines in atherosclerosis and anti-inflammatory prevention of atherosclerosis were searched in PubMed Database from their respective inceptions until October 2015. Sections “The role of infl…

Male0301 basic medicine3003Anti-Inflammatory AgentsPharmaceutical ScienceInflammation030204 cardiovascular system & hematologyBioinformaticsProinflammatory cytokineAnti-Cytokine TherapyDouble blind03 medical and health sciences0302 clinical medicineDouble-Blind MethodDrug DiscoverymedicineAnimalsHumansInterleukin 6InflammationPharmacologybiologyTraditional medicinebusiness.industryMedicine (all)Drug Discovery3003 Pharmaceutical ScienceAtherosclerosisComplementary and Alternative Medicine2708 DermatologyHerbal preparationClinical trial030104 developmental biologyComplementary and alternative medicineAtherosclerosis preventionDisease Progressionbiology.proteinCytokinesHerbal preparationsAtherosclerosis preventionMolecular MedicinePlant Preparationsmedicine.symptomAnti-cytokine therapybusiness
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Deregulation of TLR4 signaling pathway characterizes Bicuspid Aortic valve syndrome

2019

AbstractBicuspid aortic valve (BAV) disease is recognized to be a syndrome with a complex and multifaceted pathophysiology. Its progression is modulated by diverse evolutionary conserved pathways, such as Notch-1 pathway. Emerging evidence is also highlighting the key role of TLR4 signaling pathway in the aortic valve pathologies and their related complications, such as sporadic ascending aorta aneurysms (AAA). Consistent with these observations, we aimed to evaluate the role of TLR4 pathway in both BAV disease and its common complication, such as AAA. To this aim, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mea…

Male0301 basic medicineAortic valveBicuspid Aortic valve syndromeHeart Valve Diseaseslcsh:MedicineDisease0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseTLR4lcsh:ScienceAortaAged 80 and overMultidisciplinarySyndromeMiddle AgedPathophysiologymedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyFemaleSignal Transductionmedicine.medical_specialtyCardiologyArticleProinflammatory cytokine03 medical and health sciencesmedicine.arteryInternal medicineAscending aortamedicineHumansbicuspid valveAgedbicuspid valve; TLR4; aortic diseaseBAV TLR4 AAATumor Necrosis Factor-alphabusiness.industryInterleukinslcsh:RSettore MED/23 - Chirurgia CardiacaValvular diseaseaortic diseasemedicine.diseaseToll-Like Receptor 4030104 developmental biologyTLR4lcsh:QbusinessComplication030217 neurology & neurosurgeryScientific Reports
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Phenotypic characterisation of pro-inflammatory monocytes and dendritic cells in peripheral arterial disease

2012

SummaryAtherosclerosis is a chronic inflammatory process involving antigen-presenting cells like monocytes and dendritic cells (DC). The aim of this study was to perform a phenotypic characterisation of these cell types in patients with different degrees of peripheral arterial disease (PAD). Sixty patients with PAD [N= 30 intermittent claudication (IC), N= 30 critical limb ischemia (CLI)] and 30 controls were included. Peripheral blood leucocytes were analysed from peripheral blood by flow cytometry using different gating strategies to directly identify and analyse monocytes, myeloid DC, (mDC) and plasmacytoid DC (pDC). PAD patients showed a significantly higher proportion of proinflammator…

Male0301 basic medicineCD14Inflammation030204 cardiovascular system & hematologyCD16Peripheral blood mononuclear cellMonocytesImmunophenotypingProinflammatory cytokinePeripheral Arterial Disease03 medical and health sciences0302 clinical medicineIschemiamedicineHumansCD40 AntigensAgedAged 80 and overCD40biologybusiness.industryExtremitiesDendritic CellsHLA-DR AntigensHematologyCritical limb ischemiaIntermittent ClaudicationMiddle AgedIntermittent claudicationBlood Cell Countbody regions030104 developmental biologyCase-Control StudiesImmunologybiology.proteinFemaleB7-2 AntigenInflammation Mediatorsmedicine.symptombusinessThrombosis and Haemostasis
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PD123319, angiotensin II type II receptor antagonist, inhibits oxidative stress and inflammation in 2, 4-dinitrobenzene sulfonic acid-induced colitis…

2019

Angiotensin II, the main effector of renin angiotensin system, plays an important role in the inflammatory process and most of its effects are mediated through the AT1 receptor activation. However, the knowledge about the AT2 receptor involvement in this process is still evolving. We previously found that in an experimental model of colitis, AT2 receptor activation can contribute to the impairment of the muscle contractility in vitro in the course of inflammation. Here, we investigated the potential alleviating effects of the in vivo treatment of PD123319 (1-[[4-(Dimethylamino)-3-methylphenyl]methyl]-5-(diphenylacetyl)-4,5,6,7- tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid ditriflu…

Male0301 basic medicineColonPyridinesmedicine.drug_classImmunologyAngiotensin II Type 2 Receptor BlockersPharmacologyAT2 receptorReceptor Angiotensin Type 2Inflammatory bowel diseaseInflammatory bowel diseaseProinflammatory cytokineContractility03 medical and health sciencesAngiotensin0302 clinical medicinemedicineAnimalsPharmacology (medical)Rats WistarColitisReceptorPharmacologyInflammationAngiotensin II receptor type 1ChemistryAngiotensin IIImidazolesColitismedicine.diseaseReceptor antagonistAngiotensin IIRatsDinitrobenzenesOxidative Stress030104 developmental biology030217 neurology & neurosurgery
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Tissue factor pathway inhibitor primes monocytes for antiphospholipid antibody-induced thrombosis

2019

Antiphospholipid antibodies (aPLs) with complex lipid and/or protein reactivities cause complement-dependent thrombosis and pregnancy complications. Although cross-reactivities with coagulation regulatory proteins contribute to the risk for developing thrombosis in patients with antiphospholipid syndrome, the majority of pathogenic aPLs retain reactivity with membrane lipid components and rapidly induce reactive oxygen species-dependent proinflammatory signaling and tissue factor (TF) procoagulant activation. Here, we show that lipid-reactive aPLs activate a common species-conserved TF signaling pathway. aPLs dissociate an inhibited TF coagulation initiation complex on the cell surface of m…

Male0301 basic medicineLipoproteinsImmunologyPlenary Paper030204 cardiovascular system & hematologyBiochemistryMonocytesThromboplastinProinflammatory cytokine03 medical and health sciencesTissue factor0302 clinical medicineTissue factor pathway inhibitorThrombinimmune system diseasesmedicineAnimalsHumansThromboplastinBlood CoagulationneoplasmsCells CulturedNADPH oxidasebiologyChemistryThrombosisCell BiologyHematologyComplement systemMice Inbred C57BL030104 developmental biologyAntibodies Antiphospholipidbiology.proteinCancer researchFemaleSignal transductionSignal Transductionmedicine.drugBlood
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