Search results for "inbred c57bl"

showing 10 items of 1287 documents

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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Lung CD11c+ cells from mice deficient in Epstein-Barr virus-induced gene 3 (EBI-3) prevent airway hyper-responsiveness in experimental asthma

2007

Epstein-Barr virus-induced gene (EBI)-3 codes for a soluble type 1 cytokine receptor homologous to the p40 subunit of IL-12 that is expressed by antigen-presenting cells following activation. Here, we analyzed the functional role of EBI-3 in a murine model of asthma associated with airway hyper-responsiveness (AHR) in ovalbumin-sensitized mice. Upon allergen challenge, EBI-3-/- mice showed less severe AHR, decreased numbers and degranulation of eosinophils and a significantly reduced number of VCAM-1+ cells in the lungs as compared to wild-type littermates. We thus analyzed lung CD11c+ cells before and after allergen challenge in these mice and found that before allergen challenge, lung CD1…

Adoptive cell transferMyeloidCell TransplantationImmunologyVascular Cell Adhesion Molecule-1CD11cCD8-Positive T-LymphocytesBiologyMinor Histocompatibility AntigensInterferon-gammaMiceImmune systemmedicineAnimalsImmunology and AllergyReceptors CytokineLungCell ProliferationMice KnockoutLungTumor Necrosis Factor-alphaEffectorDegranulationInterferon-alphaDendritic CellsSTAT4 Transcription Factorrespiratory systemInterleukin-12AsthmaCD11c AntigenInterleukin-10respiratory tract diseasesEosinophilsMice Inbred C57BLmedicine.anatomical_structureImmunologyInterleukin-4Bronchial HyperreactivityInterleukin-5T-Box Domain ProteinsCytokine receptorBronchoalveolar Lavage FluidEuropean Journal of Immunology
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RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F.

2008

Background and Aims IL-17–producing CD4 + T-helper cells (Th17) contribute to chronic autoimmune inflammation in the brain, and levels of Th17-derived cytokines increase in patients with colitis, suggesting a role in pathogenesis. We analyzed the roles of Th17 cells and the transcription factor retinoic acid receptor-related organ receptor (ROR)γ, which regulates Th17 differentiation, in chronic intestinal inflammation. Methods Using an adoptive transfer model of colitis, we compared the colitogenic potential of wild-type, interleukin-17A (IL-17A)–, IL-17F–, IL-22–, and RORγ-deficient CD4 + CD25 − T cells in RAG1-null mice. Results Adoptive transfer of IL-17A–, IL-17F–, or IL-22–deficient T…

Adoptive cell transferNeutrophilsReceptors Retinoic Acidmedicine.medical_treatmentBiologyInflammatory bowel diseasePathogenesisMiceInterferonCell MovementmedicineAnimalsIL-2 receptorColitisCells CulturedReceptors Thyroid HormoneHepatologyInterleukinsInterleukin-17GastroenterologyDendritic CellsT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisAdoptive TransferMice Inbred C57BLCytokineImmunologyChronic Diseasebiology.proteinCytokinesAntibodymedicine.drugGastroenterology
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Melanomas resist T-cell therapy through inflammation-induced reversible dedifferentiation.

2012

Adoptive cell transfer therapies (ACTs) with cytotoxic T cells that target melanocytic antigens can achieve remissions in patients with metastatic melanomas, but tumours frequently relapse. Hypotheses explaining the acquired resistance to ACTs include the selection of antigen-deficient tumour cell variants and the induction of T-cell tolerance. However, the lack of appropriate experimental melanoma models has so far impeded clear insights into the underlying mechanisms. Here we establish an effective ACT protocol in a genetically engineered mouse melanoma model that recapitulates tumour regression, remission and relapse as seen in patients. We report the unexpected observation that melanoma…

Adoptive cell transfermedicine.medical_treatmentCellular differentiationT cellBiologyProinflammatory cytokineMiceAntigenCell Line TumormedicineTumor MicroenvironmentCytotoxic T cellAnimalsHumansMelanomaCell ProliferationInflammationMultidisciplinaryTumor Necrosis Factor-alphaMelanomaCell DifferentiationImmunotherapyCell Dedifferentiationmedicine.diseaseAdoptive TransferMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureImmunologyImmunotherapyNeoplasm TransplantationT-Lymphocytes Cytotoxicgp100 Melanoma AntigenNature
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Therapeutic Vaccination of Hematopoietic Cell Transplantation Recipients Improves Protective CD8 T-Cell Immunotherapy of Cytomegalovirus Infection

2021

Reactivation of latent cytomegalovirus (CMV) endangers the therapeutic success of hematopoietic cell transplantation (HCT) in tumor patients due to cytopathogenic virus spread that leads to organ manifestations of CMV disease, to interstitial pneumonia in particular. In cases of virus variants that are refractory to standard antiviral pharmacotherapy, immunotherapy by adoptive cell transfer (ACT) of virus-specific CD8+ T cells is the last resort to bridge the “protection gap” between hematoablative conditioning for HCT and endogenous reconstitution of antiviral immunity. We have used the well-established mouse model of CD8+ T-cell immunotherapy by ACT in a setting of experimental HCT and mu…

Adoptive cell transfermedicine.medical_treatmentImmunologyCytomegalovirusCD8-Positive T-LymphocytesLymphocyte ActivationCD8+ T cellsVirusCytomegalovirus VaccinesImmunocompromised HostAntigenvaccineMHC class ImedicineImmunology and AllergyCytotoxic T cellAnimalsCells Culturedadoptive cell transferCell ProliferationOriginal ResearchHCMV dense bodiesbiologybusiness.industryVaccinationHematopoietic Stem Cell TransplantationImmunotherapyRC581-607VirologyAdoptive TransferTransplantationMice Inbred C57BLantiviral protectionT cell primingDisease Models AnimalT cell receptor transgenic cellsCytomegalovirus InfectionsHost-Pathogen Interactionsbiology.proteinFemaleVirus Activationsubviral particlesImmunologic diseases. AllergybusinessCD8Frontiers in Immunology
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B?cells are not required for T?cell priming in low zone tolerance to contact allergens and contact hypersensitivity

2004

Low zone tolerance (LZT) to contact allergens is induced by epicutaneous exposure to haptens in subsensitizing doses resulting in an inhibition of contact hypersensitivity (CHS), which, in contrast, occurs after sensitization with immunogenic doses of allergens. Performing the protocol of tolerance induction resulted in robust LZT to allergens in B cell-deficient mice in vivo, indicating that B cells are not required for the induction and effector phase of LZT. However, CHS reactions in vivo were restricted in B cell-deficient mice as compared to wild-type (WT) mice. In contrast, analysis of hapten-specific T cell activation in vitro revealed a strong proliferative response of T cells deriv…

Adoptive cell transfermedicine.medical_treatmentT cellImmunologyPriming (immunology)Picryl ChlorideCD8-Positive T-LymphocytesBiologyDermatitis ContactLymphocyte ActivationInterferon-gammaMiceAdjuvants ImmunologicImmune TolerancemedicineAnimalsImmunology and AllergySensitizationB cellCell ProliferationMice KnockoutB-Lymphocytesintegumentary systemInterleukinsOxazoloneAllergensAdoptive TransferMice Inbred C57BLTolerance inductionCytokinemedicine.anatomical_structureImmunologyLymph NodesCD8European Journal of Immunology
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The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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Dimethyl fumarate treatment restrains the antioxidative capacity of T cells to control autoimmunity

2021

Abstract Dimethyl fumarate, an approved treatment for relapsing-remitting multiple sclerosis, exerts pleiotropic effects on immune cells as well as CNS resident cells. Here, we show that dimethyl fumarate exerts a profound alteration of the metabolic profile of human CD4+ as well as CD8+ T cells and restricts their antioxidative capacities by decreasing intracellular levels of the reactive oxygen species scavenger glutathione. This causes an increase in mitochondrial reactive oxygen species levels accompanied by an enhanced mitochondrial stress response, ultimately leading to impaired mitochondrial function. Enhanced mitochondrial reactive oxygen species levels not only result in enhanced T…

AdultCD4-Positive T-LymphocytesMaleDimethyl FumarateT cellAutoimmunityCD8-Positive T-Lymphocytesmedicine.disease_causeAntioxidantsCohort StudiesMiceYoung Adultchemistry.chemical_compoundMultiple Sclerosis Relapsing-RemittingImmune systemmedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesDimethyl fumarateExperimental autoimmune encephalomyelitisGlutathioneMiddle Agedmedicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryFemaleNeurology (clinical)Immunosuppressive AgentsOxidative stressCD8Brain
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Identification of CD4 T-Cell Epitopes in Soluble Liver Antigen/Liver Pancreas Autoantigen in Autoimmune Hepatitis

2008

Background & Aims Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease associated with autoantibodies and liver-infiltrating lymphocytes. Although autoantibodies are tested routinely to diagnose and classify AIH, liver-infiltrating lymphocytes are regarded as the primary factor for disease pathogenesis. The purpose of this study was to identify and characterize autoantigenic peptides within human AIH-specific soluble liver antigen/liver pancreas antigen (SLA/LP) that are targeted by CD4 + T cells and restricted by the disease susceptibility gene HLA-DRB1*0301. Methods HLA-DRB1*0301 transgenic mice were immunized with SLA/LP. Antibody and T-cell responses were analyzed with SLA…

AdultCD4-Positive T-LymphocytesMaleEpitopes T-LymphocyteMice TransgenicAutoimmune hepatitisBiologyAutoantigensPeripheral blood mononuclear cellArticleEpitopeImmunoenzyme TechniquesMiceYoung AdultLiver diseaseimmune system diseasesmedicineAnimalsHumansAgedAutoantibodiesHepatologymedicine.diagnostic_testELISPOTGastroenterologyAutoantibodyMiddle Agedmedicine.diseaseVirologyMice Inbred C57BLDisease Models AnimalHepatitis AutoimmuneImmunoassayImmunologybiology.proteinFemaleAntibodyGastroenterology
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