Search results for "T cell"

showing 10 items of 2228 documents

Increasing Functional Avidity of T Cell Receptor (TCR)-Redirected T Cells by Removing Defined N-Glycoslyation Sites in the Constant Domain of Introdu…

2007

Abstract Adoptive transfer of T lymphocytes transduced with a TCR to impart tumor reactivity has been reported as potential strategy to redirect immune responses to target cancer cells. However, the affinities of most TCRs specific for shared tumor antigens that can be isolated are usually low, in part reflecting the nature of the targeted tumor antigens which are self-proteins. Thus strategies that can increase the affinity or functional avidity of TCRs to be used in therapy to transduce T cells might be therapeutically beneficial. However, current strategies for increasing TCR affinity require extensive and usually random mutagenesis followed by screening the many derived mutations, and m…

Adoptive cell transferChemistryImmunologyT-cell receptorhemic and immune systemschemical and pharmacologic phenomenaCell BiologyHematologyBiochemistryCell biologyImmune systemAntigenCancer cellCytotoxic T cellAvidityCD8Blood
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Genetic proof for the transient nature of the Th17 phenotype

2010

IL-17-producing CD4(+) T cells (Th17) have been classified as a new T helper cell subset. Using an IL-17 fate mapping mouse strain, which genetically fixes the memory of IL-17 expression, we demonstrate that IL-17A/F-expressing T helper cells generated either in vitro or in vivo are not a stable T-cell subset. Upon adoptive transfer of IL-17F-reporter-positive Th17 cells to RAG-deficient or WT animals, encephalitogenic Th17 cells partially lose IL-17 expression and upregulate IFN-γ. Additionally, we show that Th1 cells can convert in vivo to IL-17A/IFN-γ-coexpressing cells in the mesenteric lymph nodes (mLN). Our data classify IL-17A and IL-17F as cytokines produced transiently in response …

Adoptive cell transferEncephalomyelitis Autoimmune ExperimentalGenes RAG-1TransgeneImmunologyReceptors Antigen T-CellMice TransgenicBiologyLymphocyte ActivationInterferon-gammaMiceInterleukin 21AntigenGenes ReporterT-Lymphocyte SubsetsIn vivomedicineAnimalsImmunology and AllergyCytotoxic T cellMesenteric lymph nodesMice KnockoutIntegrasesCell DifferentiationT helper cellTh1 CellsAdoptive TransferCell biologyMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationImmunologyTh17 CellsEuropean Journal of Immunology
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T cells expressing a chimeric antigen receptor that binds hepatitis B virus envelope proteins control virus replication in mice.

2013

Background & Aims Antiviral agents suppress hepatitis B virus (HBV) replication but do not clear the infection. A strong effector T-cell response is required to eradicate HBV, but this does not occur in patients with chronic infection. T cells might be directed toward virus-infected cells by expressing HBV-specific receptors and thereby clear HBV and help to prevent development of liver cancer. In mice, we studied whether redirected T cells can engraft after adoptive transfer, without prior T-cell depletion, and whether the large amounts of circulating viral antigens inactivate the transferred T cells or lead to uncontrolled immune-mediated damage. Methods CD8 + T cells were isolated from m…

Adoptive cell transferHepatitis B virusRecombinant Fusion ProteinsReceptors Antigen T-CellMice TransgenicAdoptive T-Cell TherapyCD8-Positive T-Lymphocytesmedicine.disease_causeVirus ReplicationInterleukin 21MiceViral Envelope ProteinsmedicineCytotoxic T cellAnimalsHumansIL-2 receptorAntigen-presenting cellHepatitis B virusCD40HepatologybiologyZAP70Gastroenterologyvirus diseasesHepatocellular CarcinomaVirologyMolecular biologyAdoptive TransferMice Inbred C57BLLiverbiology.proteinImmunotherapyChronic Hepatitis BGastroenterology
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Cytomegalovirus Misleads Its Host by Priming of CD8 T Cells Specific for an Epitope Not Presented in Infected Tissues

2003

Cytomegaloviruses (CMVs) code for several proteins that inhibit the presentation of antigenic peptides to CD8 T cells. Although the molecular mechanisms of CMV interference with the major histocompatibility complex class I pathway are long understood, surprisingly little evidence exists to support a role in vivo. Here we document the first example of the presentation of an antigenic peptide being blocked by a CMV immune evasion protein in organs relevant to CMV disease. Although this Db-restricted peptide, which is derived from the antiapoptotic protein M45 of murine CMV (mCMV), is classified as an immunodominant peptide based on response magnitude and long-term memory, adoptive transfer of…

Adoptive cell transferImmunologyMutantCytomegalovirusPriming (immunology)PeptideCD8-Positive T-LymphocytesBiologyLymphocyte ActivationMajor histocompatibility complexEpitopeImmune systemHumansImmunology and AllergyCytotoxic T cellimmune evasionchemistry.chemical_classificationimmune controlimmunodominanceImmunomagnetic SeparationBrief Definitive Reportvirus diseasesAdoptive TransferVirologyantigen presentationchemistryCytomegalovirus InfectionsImmunologybiology.proteincross-primingImmunologic MemoryJournal of Experimental Medicine
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Contribution of IL-17-producing {gamma}{delta} T cells to the efficacy of anticancer chemotherapy.

2011

IL-17 production by γδ T cells is required for tumor cell infiltration by IFN-γ–producing CD8+ T cells and inhibition of tumor growth in response to anthracyclines.

Adoptive cell transferMESH : AgedMESH : Equipment DesignCD8-Positive T-LymphocytesMESH: CatheterizationInterleukin-23MESH: Long-Term CareMice0302 clinical medicineMESH : CatheterizationT-Lymphocyte SubsetsMESH: NursingImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyInterferon gammaMESH: Quality of Health CareMESH: Professional Review OrganizationsMESH: AgedMESH : Gels0303 health sciencesMice Inbred BALB CCell DeathInterleukin-17MESH : Methylene BlueMESH : Quality of Health CareReceptors Antigen T-Cell gamma-deltaChemotherapy regimenMESH: Transplantation Autologous3. Good healthMESH: Cosmetic TechniquesTreatment Outcomemedicine.anatomical_structureMESH : Cadaver[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunogenic cell deathSarcoma ExperimentalInterleukin 17MESH : DissectionMESH : Long-Term CareMESH: Nursing CareMESH: Adipose Tissuemedicine.drugSignal TransductionMESH : Transplantation Autologous[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Feasibility StudiesMESH: GelsT cellMESH : MaleImmunologyMESH: DissectionAntineoplastic AgentsBiologyMESH : NursingMESH : Adipose TissueArticleMESH : Facial Muscles03 medical and health sciencesInterferon-gammaLymphocytes Tumor-InfiltratingImmune systemAntigenCell Line TumorMESH: Patient Care PlanningmedicineMESH: CadaverAnimalsMESH : Patient Care Planning030304 developmental biologyMESH: Humansbusiness.industryMESH: Facial MusclesT-cell receptorMESH : HumansCorrectionMESH: MaleMice Inbred C57BLMESH : Cosmetic TechniquesDoxorubicinImmunologyCancer researchMESH : Nursing CareMESH : Professional Review OrganizationsbusinessMESH: Feasibility StudiesCD8030215 immunologyMESH: Methylene BlueMESH: Equipment Design
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Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
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Subdominant CD8 T-Cell Epitopes Account for Protection against Cytomegalovirus Independent of Immunodomination▿ †

2008

ABSTRACTCytomegalovirus (CMV) infection continues to be a complication in recipients of hematopoietic stem cell transplantation (HSCT). Preexisting donor immunity is recognized as a favorable prognostic factor for the reconstitution of protective antiviral immunity mediated primarily by CD8 T cells. Furthermore, adoptive transfer of CMV-specific memory CD8 T (CD8-TM) cells is a therapeutic option for preventing CMV disease in HSCT recipients. Given the different CMV infection histories of donor and recipient, a problem may arise from an antigenic mismatch between the CMV variant that has primed donor immunity and the CMV variant acquired by the recipient. Here, we have used the BALB/c mouse…

Adoptive cell transferMuromegalovirusImmunologyEpitopes T-LymphocyteBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexMicrobiologyVirusEpitopeMiceViral ProteinsAntigenBetaherpesvirinaeVirologyCytotoxic T cellAnimalsCells CulturedMice Inbred BALB CImmunodominant Epitopesvirus diseasesHerpesviridae InfectionsFibroblastsbiology.organism_classificationVirologyAdoptive TransferDisease Models AnimalKineticsInsect ScienceImmunologybiology.proteinPathogenesis and ImmunityFemaleCD8
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Highly protective in vivo function of cytomegalovirus IE1 epitope-specific memory CD8 T cells purified by T-cell receptor-based cell sorting.

2005

ABSTRACTReconstitution of antiviral CD8 T cells is essential for controlling cytomegalovirus (CMV) infection after bone marrow transplantation. Accordingly, polyclonal CD8 T cells derived from BALB/c mice infected with murine CMV protect immunocompromised adoptive transfer recipients against CMV disease. The protective population comprises CD8 T cells with T-cell receptors (TCRs) specific for defined and for as-yet-unknown viral epitopes, as well as a majority of nonprotective cells with unrelated specificities. Defined epitopes include IE1/m123 and m164, which are immunodominant in terms of the magnitude of the CD8 T-cell response, and a panel of subordinate epitopes (m04, m18, M45, M83, a…

Adoptive cell transferMuromegalovirusReceptors Antigen T-Cell alpha-betaImmunologyEpitopes T-LymphocyteImmunodominanceCell SeparationBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexMicrobiologyEpitopeImmediate-Early ProteinsMiceViral ProteinsVirologyCytotoxic T cellAnimalsMice Inbred BALB CImmunodominant EpitopesT-cell receptorvirus diseasesHerpesviridae InfectionsCell sortingFlow CytometryVirologyMolecular biologyAdoptive TransferDisease Models AnimalInsect Sciencebiology.proteinPathogenesis and ImmunityImmunologic MemoryCD8Journal of virology
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Phenotype, Function, and Safety of a p53 TCR Bicistronic GMP-Suitable Retroviral Construct.

2006

Abstract Malignant transformation of normal cells is frequently correlated with the involvement of so called tumor-associated antigens (TAA). Such proteins, that are often overexpressed in tumor cells, can be recognized by cytotoxic CD8+ T cells (CTL) if presented as peptides on MHC (Major-Histocompatibility-Complex)-class I molecules. Due to self-tolerance mechanisms, the peripheral T cell repertoire is devoid of efficient TAA-specific, tumor-reactive CTL with high affinity, limiting the successful development of antigen-specific immunotherapeutic strategies based on such tumor-reactive T cells. The aim of this project is the preclinical development of an adoptive immunotherapy against p53…

Adoptive cell transferbiologyT cellImmunologyT-cell receptorCell BiologyHematologyDendritic cellMajor histocompatibility complexBiochemistryMolecular biologyCTL*medicine.anatomical_structurebiology.proteinCancer researchmedicineCytotoxic T cellCD8Blood
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p53 Immunotherapy of Cancer

2012

Mutation and overexpression of the p53 tumor suppressor protein are the most common genetic alterations in human cancers. Peptides derived from non-mutated (wild type, wt) and mutated p53-molecules, processed and presented in the context of major histocompatibility complex (MHC) molecules by tumor cells for T-cell recognition, could serve as broad targets for cancer immunotherapy. Isolating p53-reactive T lymphocytes in healthy donors or patients has been hampered by the fact that most individuals display a peripheral p53-reactive T-cell repertoire that is devoid of high-avidity MHC class I-restricted cytotoxic T lymphocytes (CTL). Only low-avidity T lymphocytes are left due to self-toleran…

Adoptive cell transferbiologymedicine.medical_treatmentT-cell receptorchemical and pharmacologic phenomenaImmunotherapyMajor histocompatibility complexAntigenMHC class Ibiology.proteinCancer researchmedicineCytotoxic T cellCD8
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