Search results for "T-Lymphocyte"

showing 10 items of 1502 documents

A role for TASK2 channels in the human immunological synapse.

2020

The immunological synapse is a transient junction that occurs when the plasma membrane of a T cell comes in close contact with an APC after recognizing a peptide from the antigen-MHC. The interaction starts when CRAC channels embedded in the T cell membrane open, flowing calcium ions into the cell. To counterbalance the ion influx and subsequent depolarization, Kv 1.3 and KCa3.1 channels are recruited to the immunological synapse, increasing the extracellular K+ concentration. These processes are crucial as they initiate gene expression that drives T cell activation and proliferation. The T cell-specific function of the K2P channel family member TASK2 channels and their role in autoimmune p…

0301 basic medicineMaleCD3 ComplexImmunological SynapsesT cellCD3T-LymphocytesImmunologyCellGene ExpressionStimulationImmunological synapseAutoimmune Diseases03 medical and health sciencesJurkat CellsMice0302 clinical medicinePotassium Channels Tandem Pore DomainCell Line TumorGene expressionmedicineExtracellularImmunology and AllergyAnimalsHumansCells CulturedKv1.3 Potassium Channelbiologyβ-tubulin ; TASK2 ; immunological synapse ; dSTORM ; T cellCell MembraneDepolarizationIntermediate-Conductance Calcium-Activated Potassium ChannelsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurebiology.proteinCalciumFemale030215 immunologyEuropean journal of immunologyReferences
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Switching to dual/monotherapy determines an increase in CD8+ in HIV-infected individuals: An observational cohort study

2018

Background The CD4/CD8 ratio has been associated with the risk of AIDS and non-AIDS events. We describe trends in immunological parameters in people who underwent a switch to monotherapy or dual therapy, compared to a control group remaining on triple antiretroviral therapy (ART). Methods We included patients in Icona who started a three-drug combination ART regimen from an ART-naïve status and achieved a viral load ≤ 50 copies/mL; they were subsequently switched to another triple or to a mono or double regimen. Standard linear regression at fixed points in time (12-24 months after the switch) and linear mixed model analysis with random intercepts and slopes were used to compare CD4 and CD8…

0301 basic medicineMaleCD4-CD8 Ratiolcsh:MedicineHIV InfectionsCD8-Positive T-LymphocytesCD4/CD8 ratio; CD8; Chronic inflammation; Dual therapy; Monotherapy; Adult; Anti-HIV Agents; CD4-CD8 Ratio; CD8-Positive T-Lymphocytes; Cohort Studies; Emtricitabine; Female; HIV Infections; Humans; Male; Middle Aged; Reverse Transcriptase Inhibitors; Tenofovir; Medicine (all)Cohort Studies0302 clinical medicineEmtricitabineHIV Infection030212 general & internal medicineMedicine (all)General MedicineChronic inflammationCD4/CD8 ratio; CD8; Chronic inflammation; Dual therapy; Monotherapy; Medicine (all)Middle AgedSettore MED/07 - Microbiologia e Microbiologia ClinicaReverse Transcriptase InhibitorReverse Transcriptase InhibitorsFemalecd4/cd8 ratio; cd8; chronic inflammation; dual therapy; monotherapy; medicine (all)Research Articlemedicine.drugCohort studyHumanAdultmedicine.medical_specialtyDual therapyCD4/CD8 ratio; CD8; Chronic inflammation; Dual therapy; Monotherapy; Adult; Anti-HIV Agents; CD4-CD8 Ratio; CD8-Positive T-Lymphocytes; Cohort Studies; Emtricitabine; Female; HIV Infections; Humans; Male; Middle Aged; Reverse Transcriptase Inhibitors; TenofovirAnti-HIV Agents030106 microbiologyCD4-CD8 RatioEmtricitabineSettore MED/17 - MALATTIE INFETTIVENO03 medical and health sciencesCD4/CD8 ratioInternal medicineLinear regressionmedicineHumansDual therapyTenofovirbusiness.industrylcsh:RAnti-HIV AgentCD8CD8-Positive T-LymphocyteMonotherapyConfidence intervalRegimenCD4/CD8 ratio; CD8; Chronic inflammation; Dual therapy; MonotherapyCD8; CD4/CD8 ratio; Chronic inflammation; Monotherapy; Dual therapyCohort StudiebusinessCD8
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Transfer of minimally manipulated CMV-specific T cells from stem cell or third-party donors to treat CMV infection after allo-HSCT.

2017

Cytomegalovirus (CMV) infection is a common, potentially life-threatening complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT). We assessed prospectively the safety and efficacy of stem cell-donor-or third-party-donor-derived CMV-specific T cells for the treatment of persistent CMV infections after allo-HSCT in a phase I/IIa trial. Allo-HSCT patients with drugrefractory CMV infection and lacking virus-specific T cells were treated with a single dose of ex vivo major histocompatibility complex-Streptamer-isolated CMV epitope-specific donor T cells. Forty-four allo-HSCT patients receiving a T-cell-replete (D+ repl; n = 28) or T-cell-depleted (D+ depl; n = 16) …

0301 basic medicineMaleCancer ResearchAdoptive cell transfermedicine.medical_treatmentT-LymphocytesCytomegalovirusT-Cell Antigen Receptor SpecificityHuman leukocyte antigenHematopoietic stem cell transplantationAntiviral AgentsImmunotherapy AdoptiveLymphocyte Depletion03 medical and health sciencesImmunocompromised HostDrug Resistance ViralmedicineHumansProspective StudiesViremiabusiness.industryGraft SurvivalHematopoietic Stem Cell Transplantationvirus diseasesHematologyImmunotherapyAllograftsVirologyTissue DonorsHistocompatibilityTransplantationHaematopoiesis030104 developmental biologyOncologyHematologic NeoplasmsHistocompatibilityMyelodysplastic SyndromesImmunologyCytomegalovirus InfectionsFemaleStem cellbusiness
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miR-21 antagonism abrogates Th17 tumor promoting functions in multiple myeloma

2020

Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis…

0301 basic medicineMaleCancer ResearchBone diseaseApoptosisBone NeoplasmsNodMice SCIDBone NeoplasmT-Lymphocytes RegulatoryTh17 Cell03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationgammopathiesMice Inbred NODmedicineTumor Cells CulturedTumor MicroenvironmentBiomarkers TumorAnimalsHumansMultiple myelomaCell ProliferationChemistryCell growthAnimalApoptosiHematologymedicine.diseasePrognosisXenograft Model Antitumor AssaysIn vitroGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCase-Control StudiesCancer researchTh17 CellsBone marrowAntagonismCase-Control StudieMultiple Myeloma
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Δ133p53α enhances metabolic and cellular fitness of TCR-engineered T cells and promotes superior antitumor immunity

2021

BackgroundTumor microenvironment-associated T cell senescence is a key limiting factor for durable effective cancer immunotherapy. A few studies have demonstrated the critical role of the tumor suppressor TP53-derived p53 isoforms in cellular senescence process of non-immune cells. However, their role in lymphocytes, in particular tumor-antigen (TA) specific T cells remain largely unexplored.MethodsHuman T cells from peripheral blood were retrovirally engineered to coexpress a TA-specific T cell receptor and the Δ133p53α-isoform, and characterized for their cellular phenotype, metabolic profile and effector functions.ResultsPhenotypic analysis of Δ133p53α-modified T cells revealed a marked …

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT cellT-LymphocytesImmunologyReceptors Antigen T-Cell2436receptorsBiologycell engineeringadoptive03 medical and health sciencesMice0302 clinical medicineantigenTIGITCancer immunotherapyAntigenCell Line TumorNeoplasmsmedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumans1506RC254-282PharmacologyImmune Cell Therapies and Immune Cell EngineeringCD28Neoplasms. Tumors. Oncology. Including cancer and carcinogensT lymphocyteImmunotherapycostimulatory and inhibitory T-cell receptorsCell biology030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisMolecular MedicineimmunotherapyCD8Journal for ImmunoTherapy of Cancer
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CD19 Isoforms Enabling Resistance to CART-19 Immunotherapy Are Expressed in B-ALL Patients at Initial Diagnosis.

2017

Supplemental Digital Content is available in the text.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT-LymphocytesEpitopes T-LymphocyteT-Cell Antigen Receptor SpecificityImmunotherapy AdoptiveEpitopeCohort StudiesExon0302 clinical medicineimmune system diseasesImmunology and AllergyMedicineProtein IsoformsChildAged 80 and overbiologyCD19CART-19B-ALLMiddle AgedPrecursor Cell Lymphoblastic Leukemia-Lymphomaepitope-lossmedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisChild PreschoolComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleClone (B-cell biology)Gene isoformAdultAdolescentRecombinant Fusion ProteinsImmunologyAntigens CD19Receptors Antigen T-CellCancer VaccinesCD1903 medical and health sciencesYoung AdultAntigenHumansAgedPharmacologybusiness.industryInfant NewbornisoformsInfantImmunotherapy030104 developmental biologyImmunologybiology.proteinClinical StudyTumor EscapeBone marrowbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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NKp46-expressing human gut-resident intraepithelial Vδ1 T cell subpopulation exhibits high antitumor activity against colorectal cancer

2019

γδ T cells account for a large fraction of human intestinal intraepithelial lymphocytes (IELs) endowed with potent anti-tumor activities. However, little is known about their origin, phenotype and clinical relevance in colorectal cancer (CRC). To determine γδ IEL gut-specificity, homing and functions, γδ T cells were purified from human healthy blood, lymph nodes, liver, skin, intestine either disease-free or affected by CRC or generated from thymic precursors. The constitutive expression of NKp46 specifically identifies a new subset of cytotoxic Vδ1 T cells representing the largest fraction of gut-resident IELs. The ontogeny and gut-tropism of NKp46pos/Vδ1 IELs depends both on distinctive …

0301 basic medicineMaleColorectal cancerImmunotherapy AdoptiveMice0302 clinical medicineSex Hormone-Binding GlobulinCytotoxic T cellAntigens LyIntestinal MucosaIntraepithelial LymphocytesInnate immunityAged 80 and overGastroenterologyAge FactorsReceptors Antigen T-Cell gamma-deltaGeneral MedicineMiddle AgedPhenotypemedicine.anatomical_structure030220 oncology & carcinogenesisDisease ProgressionFemaleColorectal NeoplasmsResearch ArticleAdultColonT cellImmunologyT cellsBiologydigestive systemColorectal cancer; Gastroenterology; Immunology; Innate immunity; T cells03 medical and health sciencesYoung AdultIleummedicineAnimalsHumansAgedNeoplasm StagingTumor microenvironmentInnate immune systemNatural Cytotoxicity Triggering Receptor 1medicine.diseaseColorectal cancer030104 developmental biologyCancer researchIntraepithelial lymphocyteHoming (hematopoietic)T-Lymphocytes Cytotoxic
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study

2017

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic …

0301 basic medicineMaleLymphocyteReceptor expressionProgrammed Cell Death 1 Receptorlcsh:MedicineCytomegalovirusGene ExpressionArtificial Gene Amplification and ExtensionPathology and Laboratory MedicineImmune ReceptorsBiochemistryPolymerase Chain ReactionMonocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesAnimal CellsT-Lymphocyte SubsetsMedicine and Health SciencesLymphocyteslcsh:ScienceAged 80 and overMultidisciplinaryImmune System ProteinsT CellsMiddle AgedAcquired immune systemFlow CytometryPrognosisShock Septicmedicine.anatomical_structurePhenotypeSpectrophotometryShock (circulatory)Cytomegalovirus InfectionsFemaleCytophotometrymedicine.symptomCellular TypesResearch ArticleSignal TransductionT cellImmune CellsImmunologyReceptors Antigen T-CellBiologyResearch and Analysis MethodsMicrobiologyImmunophenotypingSepsis03 medical and health sciencesImmune systemSigns and SymptomsDiagnostic MedicineSepsisVirologymedicineHumansMolecular Biology TechniquesMolecular BiologyAgedBlood CellsSeptic shocklcsh:RBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyHLA-DR Antigensmedicine.diseaseViral ReplicationT Cell Receptors030104 developmental biologyCase-Control StudiesImmunologylcsh:QBiomarkersPLoS ONE
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