Search results for " T-Cell"

showing 10 items of 320 documents

Human ectonucleotidase-expressing CD25 high Th17 cells accumulate in breast cancer tumors and exert immunosuppressive functions

2015

IF 7.644; International audience; Th17 cells contribute to the development of some autoimmune and allergic diseases by driving tissue inflammation. However, the function of Th17 cells during cancer progression remains controversial. Here, we show that human memory CD25(high) Th17 cells suppress T cell immunity in breast cancer. Ectonucleotidase-expressing Th17 cells accumulated in breast cancer tumors and suppressed CD4(+) and CD8(+) T cell activation. These cells expressed both Ror gamma t and Foxp3 genes and secreted Th17 related cytokines. We further found that CD39 ectonucleotisase expression on tumor-infiltrating Th17 cells was driven by TGF-beta and IL-6. Finally, immunohistochemical …

0301 basic medicineAdenosineT cellImmunologyGeneration[SDV.CAN]Life Sciences [q-bio]/Cancerchemical and pharmacologic phenomenaBiology[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciencesInterleukin 21Immune systembreast cancerCancer stem cellmedicineCd73Immunology and AllergyChemotherapy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyIL-2 receptorRegulatory T-CellsSuppressionCarcinomaFOXP3hemic and immune systemsSuicide gene3. Good healthReceptor Ccr6030104 developmental biologymedicine.anatomical_structurePhenotypeOncologyImmunologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyTh17prognosisectonucleotidase
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Mutanome directed cancer immunotherapy

2015

Somatic mutations are important drivers of cancer development. Accumulating evidence suggests that a significant subset of mutations result in neo-epitopes recognized by autologous T cells and thus may constitute the Achilles' heel of tumor cells. T cells directed against mutations have been shown to have a key role in clinical efficacy of potent cancer immunotherapy modalities, such as adoptive transfer of autologous tumor infiltrating lymphocytes and immune checkpoint inhibitors. Whereas these findings strengthen the idea of a prominent role of neo-epitopes in tumor rejection, the systematic therapeutic exploitation of mutations was hampered until recently by the uniqueness of the reperto…

0301 basic medicineAdoptive cell transferSomatic cellT-Lymphocytesmedicine.medical_treatmentImmune checkpoint inhibitorsImmunology03 medical and health sciences0302 clinical medicineCancer immunotherapyAntigens NeoplasmNeoplasmsAnimalsHumansImmunology and AllergyMedicineClinical efficacybusiness.industryAutologous T-cellsImmune recognition030104 developmental biology030220 oncology & carcinogenesisTumor rejectionMutationImmunologyImmunotherapybusiness
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γδ cells and tumor microenvironment: A helpful or a dangerous liason?

2017

Abstract γδ T cells are a subset of T lymphocytes that have been implicated in immunosurveillance against infections and tumors. γδ T cells are endowed with antitumor activities, and hence several γδ T cell-based small-scale clinical trials have been conducted either by in vivo activation by intravenous administration of aminobiphosphonates or by adoptive transfer of in vitro expanded γδ T cells. Although both these strategies have yielded promising results, there are a number of limitations associated with each of them which, if overcome may help to further improve efficacy. One of the most important limits is the possible polarization of tumor-infiltrating γδ T cells toward different γδ T…

0301 basic medicineAdoptive cell transferT cellmedicine.medical_treatmentT-LymphocytesImmunologyPopulationBiology03 medical and health sciencesCancer immunotherapytumor-infiltrating lymphocyteNeoplasmsmedicineTumor MicroenvironmentImmunology and AllergyHumanseducationγδ T cellTumor microenvironmenteducation.field_of_studyTumor-infiltrating lymphocytesReceptors Antigen T-Cell gamma-deltaCell BiologyIn vitroImmunosurveillance030104 developmental biologymedicine.anatomical_structureT-LymphocyteCancer researchNeoplasmtumor microenviromentHumanJournal of leukocyte biology
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Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity

2016

Regulatory T (Treg) cells expressing Foxp3 transcripton factor are essential for immune homeostasis. They arise in the thymus as a separate lineage from conventional CD4+Foxp3- T (Tconv) cells. Here, we show that the thymic development of Treg cells depends on the expression of their endogenous cognate self-antigen. The formation of these cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negatively affected. Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerate recognition of distinct antigens. These distinct modes of development were associated with the expressi…

0301 basic medicineCell typeCancer ResearchEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosis[SDV]Life Sciences [q-bio]ImmunologyReceptors Antigen T-CellEndogenyT-Cell Antigen Receptor Specificitychemical and pharmacologic phenomenaThymus GlandBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesMice0302 clinical medicineAntigenT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsHumansAvidityCTLA-4 AntigenReceptorClonal Selection Antigen-MediatedCells CulturedMice KnockoutCell growthFOXP3Forkhead Transcription Factorshemic and immune systemsPeptide Fragments[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyMyelin-Oligodendrocyte Glycoprotein030215 immunology
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Signalling strength determines proapoptotic functions of STING

2017

Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prev…

0301 basic medicineCell typeLeukemia T-CellTranscription Geneticmedicine.medical_treatmentScienceCellsT-LymphocytesGeneral Physics and AstronomyActivationApoptosisInnate Immune SensorBiologyCytosolic DnaCgasGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCyclic Gmp-Amp[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineAnimalsReceptorlcsh:ScienceMultidisciplinaryInnate immune systemEffectorQ2nd-MessengerMembrane ProteinsGeneral ChemistryHedgehog signaling pathwayeye diseases3. Good healthCell biologyMice Inbred C57BLSting030104 developmental biologyCytokineDi-GmpImmunologylcsh:QInterferon Regulatory Factor-3Signal transductionTumor Suppressor Protein p53InfectionProtein BindingSignal TransductionNature Communications
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T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita

2016

AbstractT cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to the effector phase of antibody-mediated autoimmune dermatoses, i.e., tissue injury and inflammation of the skin, has not been investigated. In this paper, we demonstrate that T cells amplify the development of autoantibody-induced tissue injury in a prototypical, organ-specific autoimmune disease, namely epidermolysis bullosa acquisita (EBA) – characterized and caused by autoantibodies targeting type VII collagen. Specifically, we show that immune complex (IC)-induced inflammation depends on the presence of T cells – a process facilitated by T cell receptor (…

0301 basic medicineEpidermolysis bullosa acquisitamedicine.medical_specialtyCollagen Type VIINeutrophilsT-LymphocytesGene ExpressionMice NudeInflammationAntigen-Antibody ComplexCell CommunicationEpidermolysis Bullosa AcquisitaArticleMice03 medical and health sciencesCricetulus0302 clinical medicinemedicineAnimalsHumansAutoantibodiesSkinAutoimmune diseaseMice Inbred BALB CMultidisciplinarybusiness.industryT-cell receptorAutoantibodyAntibodies MonoclonalReceptors Antigen T-Cell gamma-deltamedicine.diseaseNatural killer T cellDermatologyImmune complexMice Inbred C57BLDisease Models Animal030104 developmental biologyLymphatic systemImmunoglobulin GImmunologyNatural Killer T-CellsLymph NodesRabbitsmedicine.symptombusinessSpleenSignal Transduction030215 immunologyScientific Reports
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Antigen-dependent competition shapes the local repertoire of tissue-resident memory CD8+ T cells.

2016

Muschaweckh et al. show that antigen presentation in the skin regulates the generation of tissue-resident memory T (TRM) cells by orchestrating local competition of antiviral CD8+ T cells, revealing a mechanism to fine-tune the repertoire of regional pools of TRM cells.

0301 basic medicineImmunologyReceptors Antigen T-CellMice TransgenicVaccinia virusCell fate determinationBiologyCD8-Positive T-LymphocytesVirusArticle31203 medical and health sciencesMice0302 clinical medicineAntigen319VacciniaImmunology and AllergyCytotoxic T cellAnimalsAntigens ViralResearch ArticlesCell growthRepertoireT-cell receptorVirology030104 developmental biologyCD8030215 immunologySignal Transduction
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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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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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