Search results for "Lymphocyte"

showing 10 items of 2280 documents

The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-…

Adjuvants Immunologic; Animals; Humans; Interleukin-13; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mice; Mice Inbred BALB C; Mice Knockout; Mice SCID; Models Biological; NFATC Transcription Factors; Oxazolone; T-LymphocytesT cellT-LymphocytesImmunologyMice SCIDBiologyLymphocyte ActivationInflammatory bowel diseaseModels BiologicalArticleOxazoloneTCIRG1chemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansColitisMice KnockoutMice Inbred BALB CInterleukin-13NFATC Transcription FactorsInterleukin-6Interleukin-17OxazoloneArticlesmedicine.diseasemedicine.anatomical_structurechemistryImmunologyInterleukin 13Cancer researchInterleukin 17The Journal of Experimental Medicine
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Induction of B-cell development in adult mice reveals the ability of bone marrow to produce B-1a cells

2009

AbstractTo study B-cell development from bone marrow (BM), we generated recombination-activating gene 1 (Rag1)–targeted mice lacking mature lymphocytes. B-cell development can be induced in such mice by B cell–specific restoration of a functional Rag1 transcription unit. Follicular and marginal zone B cells populated the spleen when Rag1 expression was permitted. Notably, the peritoneal cavity was dominated by bona fide B-1a cells, as judged by surface markers and functional properties. These BM-derived B-1a cells exhibited a polyclonal VDJ repertoire with substantial N nucleotide insertions. Nevertheless, physiologic frequencies of phosphatidylcholine-specific B cells were detected. Import…

Adoptive cell transfer1303 BiochemistryGenes RAG-1Immunology2720 HematologyB-Lymphocyte SubsetsSpleenBone Marrow CellsEnzyme-Linked Immunosorbent AssayMice Transgenic610 Medicine & healthBiology10263 Institute of Experimental ImmunologyBiochemistryPolymerase Chain ReactionRecombination-activating gene1307 Cell BiologyPeritoneal cavityMicemedicineAnimalsB cellB-Lymphocytes2403 ImmunologyStem CellsCell DifferentiationCell BiologyHematologyMarginal zoneFlow CytometryMolecular biologyAdoptive Transfermedicine.anatomical_structureImmunoglobulin MImmunologybiology.protein570 Life sciences; biologyBone marrow
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Functional Analyses of Human T Cell Extravasation in a Humanized NOD/SCID/IL2Rγcnull Transplantation Model.

2009

Abstract Abstract 2448 Poster Board II-425 Donor lymphocyte graft engineering to avoid graft-versus-host (GVH) reactivity while improving graft-versus-leukemia (GVL) immunity remains of central interest in allogeneic hematopoietic stem cell transplantation (HSCT). However, appropriate models to evaluate experimental concepts of donor lymphocyte allograft engineering in vivo are missing. We, therefore, established a human-murine chimeric transplantation model using immunodeficient NOD/SCID/IL2Rγcnull (NSG) mice to evaluate GVH reactivity of human T cell grafts in vivo. Moreover, since mechanisms of immune functions resembling human GVH immunity have not yet been addressed in detail in these …

Adoptive cell transferCell adhesion moleculeChemistryT cellLymphocyteImmunologyCell BiologyHematologyCD49dBiochemistryTransplantationImmune systemmedicine.anatomical_structureCancer researchmedicineLymphocyte function-associated antigen 1Blood
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Induction of the anti-ergotypic response.

1993

The injection of syngeneic activated T cells into rodents can induce a T cell response against activation markers of the T cells, ergotopes. The responding anti-ergotypic T cells have been shown to suppress experimental autoimmune encephalomyelitis (EAE). This paper reports the characteristics of the anti-ergotypic response. It was found that irradiated activated T cells were as good as untreated living activated T cells in inducing anti-ergotypic cells in vivo. Glutardialdehyde-fixed (0.3%) cells were poor stimulators in vivo and non-stimulatory in vitro. Dilution of glutardialdehyde to 0.003% before fixation preserved the stimulatory capacity in vitro. Fixation or irradiation of T cells a…

Adoptive cell transferCellular immunityT cellT-LymphocytesImmunologyDose-Response Relationship ImmunologicBiologyIn Vitro TechniquesLymphocyte ActivationEpitopeImmune systemIn vivomedicineImmunology and AllergyAnimalsAutoantibodiesProteinsGeneral MedicineT lymphocyteMolecular biologyIn vitroRatsKineticsmedicine.anatomical_structureSolubilityRats Inbred LewImmunologyFemaleInternational immunology
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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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Lack of requirement for CD8+ cells in recovery from and resistance to experimental autoimmune encephalomyelitis.

1995

Abstract Experimental autoimmune encephalomyelitis (EAE) is a model of T-cell mediated autoimmune disease. Active disease is mediated by myelin basic protein specific CD4+T-cells, whose adoptive transfer can also induce passive disease. In the Lewis rat EAE is a transient disease inducing lasting resistance to rechallenge. The mechanisms of recovery and resistance are poorly understood. CD8+suppressor T-cells have mostly been thought to be central, especially in resistance to reinduction of the disease. In this study we showed by complete depletion of CD8+cells that this subset does not influence either recovery or resistance to EAE in the Lewis rat. This was further confirmed by depleting …

Adoptive cell transferEncephalomyelitis Autoimmune Experimentalmedicine.drug_classEncephalomyelitisImmunologyCD4-CD8 RatioCD8-Positive T-LymphocytesMonoclonal antibodyLymphocyte DepletionImmunopathologymedicineImmunology and AllergyAnimalsAutoimmune diseasebiologyExperimental autoimmune encephalomyelitisAntibodies Monoclonalmedicine.diseaseImmunity InnateMyelin basic proteinRatsRats Inbred LewImmunologybiology.proteinFemaleCD8Journal of autoimmunity
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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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