Search results for "Interferon-γ"

showing 8 items of 8 documents

The Immunomodulatory Properties of the Human Amnion-Derived Mesenchymal Stromal/Stem Cells Are Induced by INF-γ Produced by Activated Lymphomonocytes…

2020

Human mesenchymal stromal/stem cells (MSCs), being immunoprivileged and having immunomodulatory ability, represent a promising tool to be applied in the field of regenerative medicine. Based on numerous in vitro evidences, the immunological effects of MSCs on immune cells could depend on different mechanisms as cell-to-cell contact and paracrine signals. Furthermore, recent studies have shown that the immunomodulatory activity of MSCs is initiated by activated immune cells; thus, their interaction represents a potential homeostatic mechanism by which MSCs regulate the immune response. MSCs also release exosomes able to give different effects, in a paracrine manner, by influencing inflammato…

0301 basic medicineProgrammed Cell Death 1 ReceptorCell CommunicationLymphocyte ActivationimmunomodulationB7-H1 AntigenMonocytes0302 clinical medicineImmunology and AllergyOriginal ResearchChemistryCell DifferentiationHealthy VolunteersI-kappa B KinaseCell biologymedicine.anatomical_structureprimed-hAMSCsMonocyte differentiationCytokinesStem celllcsh:Immunologic diseases. AllergyStromal cellT cellPrimary Cell CultureImmunologyregenerative medicineexosomesInterferon-gamma03 medical and health sciencesParacrine signallingImmune systeminterferon-γmedicineHumansImmunologic FactorsAmnionhuman amnion-derived mesenchymal stem cellsCell ProliferationImmunosuppression TherapyPDL-1Mesenchymal stem cellImmunityM2-like monocytesMesenchymal Stem CellsCoculture TechniquesMicrovesiclesMicroRNAs030104 developmental biologyLeukocytes Mononuclearlcsh:RC581-607Interferon Regulatory Factor-1030215 immunologyFrontiers in Immunology
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INFγ stimulates arginine transport through system y+L in human monocytes

2004

Freshly isolated human monocytes transport L-arginine mostly through a sodium independent, NEM insensitive pathway inhibited by L-leucine in the presence, but not in the absence of sodium. Interferon-gamma (IFNgamma) stimulates this pathway, identifiable with system y+L, and markedly enhances the expression of SLC7A7, the gene that encodes for system y+L subunit y+LAT1, but not of SLC7A6, that codes for the alternative subunit y+LAT2. System y+ plays a minor role in arginine uptake by monocytes and the expression of system y+-related genes, SLC7A1 and SLC7A2, is not changed by IFNgamma. These results demonstrate that system y+L is sensitive to IFNgamma.

ArginineSodiumProtein subunitBiophysicschemistry.chemical_elementBiologyLPI - Lysinuric protein intoleranceArginineMonocyteBiochemistryMonocytesInterferon-gammaInterferon γLeucineStructural BiologyArginine transportSystem y+L.GeneticsmedicineHumansMolecular BiologyGeneLysinuric protein intoleranceCells CulturedArginine transportReverse Transcriptase Polymerase Chain ReactionFusion Regulatory Protein 1 Light ChainsMonocyteSodiumAmino Acid Transport System y+LBiological TransportCell BiologyMolecular biologyRecombinant ProteinsKineticsmedicine.anatomical_structurechemistryEthylmaleimideAmino Acid Transport Systems BasicInterferon-γFEBS Letters
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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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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Recovery of Varicella-Zoster Virus–Specific T Cell Immunity after T Cell–Depleted Allogeneic Transplantation Requires Symptomatic Virus Reactivation

2008

Abstract Reactivated varicella-zoster virus (VZV) infection causes herpes zoster and commonly occurs after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Because VZV-specific T cell immunity is essential to prevent virus reactivation, we developed an interferon-γ enzyme-linked immunosorbent spot (ELISPOT) assay for the sensitive detection of VZV-reactive T cells at the single-cell level ex vivo. We used this assay to monitor the frequency of VZV-reactive T cells in 17 seropositive patients during the first year after T cell–depleted allo-HSCT. The patients did not receive anti-herpesvirus prophylaxis after stem cell engraftment. Independent of the magnitude of transferred d…

MaleHerpesvirus 3 HumanT-Lymphocytesvirusesmedicine.medical_treatmentT cellHerpes zosterHematopoietic stem cell transplantationmedicine.disease_causeLymphocyte DepletionVirusImmunitymedicineHumansTransplantation HomologousImmunity CellularTransplantationintegumentary systembusiness.industryELISPOTVaccinationHematopoietic Stem Cell TransplantationELISPOTVaricella zoster virusvirus diseasesViral VaccinesRecovery of FunctionHematologybiochemical phenomena metabolism and nutritionVirologyTransplantationmedicine.anatomical_structureHematologic NeoplasmsImmunologyVaricella-zoster virusFemaleVirus ActivationInterferon-γStem cellT cell depletionbusinessBiology of Blood and Marrow Transplantation
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Gliadin activates arginase pathway in RAW264.7 cells and in human monocytes

2014

AbstractCeliac disease (CD) is an autoimmune enteropathy triggered in susceptible individuals by the ingestion of gliadin-containing grains. Recent studies have demonstrated that macrophages play a key role in the pathogenesis of CD through the release of inflammatory mediators such as cytokines and nitric oxide (NO). Since arginine is the obliged substrate of iNOS (inducible nitric oxide synthase), the enzyme that produces large amount of NO, the aim of this work is to investigate arginine metabolic pathways in RAW264.7 murine macrophages after treatment with PT-gliadin (PTG) in the absence and in the presence of IFNγ. Our results demonstrate that, besides strengthening the IFNγ-dependent …

OrnithineArginineBlotting WesternNitric Oxide Synthase Type IIOrnithine DecarboxylaseReal-Time Polymerase Chain ReactionArginineMonocytesGliadinOrnithine decarboxylaseInterferon-gammaMicechemistry.chemical_compoundmedicineAnimalsHumansCeliac diseaseMacrophageRNA MessengerMolecular BiologyCells CulturedArginasebiologyReverse Transcriptase Polymerase Chain ReactionMacrophagesMonocytenutritional and metabolic diseasesNitric oxideOrnithineMolecular biologyPeptide FragmentsNitric oxide synthaseArginasemedicine.anatomical_structureBiochemistrychemistrybiology.proteinMolecular MedicineInterferon-γGliadinBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Alfavīrusu vektoru izstrāde makrofāgu aktvācijai vēža imunoterapijā

2016

Audzēju-iefiltrējošiem makrofāgiem piemīt gan spēja veicināt audzēja attīstību, gan inhibēt, attiecībā no to aktivācijas stāvokļa. In vitro pētījumos ir ticis parādīts, ka, iedarbojoties ar interferonu-g (IFN-γ) kopā ar Toll-like receptora (TLR) ligandu, tika ierosināts M1 makrofāgu fenotips, kas tiek asociēts ar audzēja iznīcināšanu. Audzēja imūnterapiju varētu nodrošināt M1 makrofāgu fenotipa inducēšana audzēju-iefiltrējošos makrofāgos. Šajā darbā mēs izvērtējām Semliki meža vīrusa (SFV) vektoru potenciālu makrofāgu aktivācijā pret vēzi. SFV tika izmantots, lai konstruētu replikācijas defektīvus konstruktus ar ieklonētiem peļu audzēja nekrozes faktora (mTNFα), peļu IFNγ un cilvēka IFNγ gē…

cancer immunotherapyrecombinant SFVmacrophage activationinterferon-γBioloģijasurvival
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Detection of natural killer T cells in mice infected with Rickettsia conorii.

2013

Little information is available regarding the role of natural killer T (NKT) cells during the early stage of Rickettsia conorii infection. Herein, C3H/HeN mice were infected with the Malish 7 strain of R. conorii. Splenocytes from these mice were analysed in the early stage of the infection by flow cytometry and compared with uninfected controls. Our results showed an increase in NKT cells in infected mice. Additionally, NKT interleukin (IL)-17(+) cells increased three days after infection, together with a concurrent decrease in the relative amount of NKT interferon (IFN)-γ(+) cells. We also confirmed a higher amount of NK IFN-γ(+) cells in infected mice. Taken together, our data showed tha…

rickettsiosis; interleukin 17; interferon-γchemical and pharmacologic phenomenaSpleenrickettsiosisBiologyBoutonneuse FeverFlow cytometryMiceInterferonmedicineAnimalsCells CulturedImmunity CellularMice Inbred C3HGeneral VeterinaryGeneral Immunology and Microbiologymedicine.diagnostic_testInterleukinGeneral Medicinemedicine.diseaseNatural killer T cellbiology.organism_classificationInterferon-γ; interleukin 17; rickettsiosisVirologyRickettsia conoriiRickettsiosismedicine.anatomical_structureImmunologyNatural Killer T-CellsInterferon-γInterleukin 17Rickettsia conoriiinterleukin 17Spleenmedicine.drugTransboundary and emerging diseases
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