Search results for "transgenic"

showing 10 items of 552 documents

Liver X Receptor–Mediated Induction of Cholesteryl Ester Transfer Protein Expression Is Selectively Impaired in Inflammatory Macrophages

2009

Objective— Cholesteryl ester transfer protein (CETP) is a target gene for the liver X receptor (LXR). The aim of this study was to further explore this regulation in the monocyte-macrophage lineage and its modulation by lipid loading and inflammation, which are key steps in the process of atherogenesis. Methods and Results— Exposure of bone marrow–derived macrophages from human CETP transgenic mice to the T0901317 LXR agonist increased CETP, PLTP, and ABCA1 mRNA levels. T0901317 also markedly increased CETP mRNA levels and CETP production in human differentiated macrophages, whereas it had no effect on CETP expression in human peripheral blood monocytes. In inflammatory mouse and human mac…

030204 cardiovascular system & hematologyMonocytesMice0302 clinical medicinepolycyclic compoundsPhospholipid Transfer ProteinsCells CulturedLiver X Receptors0303 health sciencesCell DifferentiationOrphan Nuclear ReceptorsUp-RegulationLipoproteins LDLmedicine.anatomical_structureABCG1Models Animalmonocytelipids (amino acids peptides and proteins)medicine.symptomCardiology and Cardiovascular MedicineOxidation-ReductionAgonistmedicine.medical_specialtymedicine.drug_classBlotting Westerncholesteryl ester transfer proteinMice TransgenicInflammationmacrophageBiology03 medical and health sciencesDownregulation and upregulationInternal medicineCholesterylester transfer proteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLiver X receptorLiver X receptorProbability030304 developmental biologyMacrophagesMonocyteAtherosclerosisCholesterol Ester Transfer Proteinscarbohydrates (lipids)EndocrinologyGene Expression RegulationinflammationABCA1Immunologybiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.

2009

The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid-beta protein precursor (AbetaPP) within the region of the amyloid-beta peptides to prevent their formation and aggregation in the brain. Members of the ADAM family (a disintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. We recently demonstrated that overexpression of ADAM10 in mice transgenic for human AbetaPP (ADAM10 x APP[V717I]) alleviated functional deficits related to Alzheimer's disease. To further demonstrate that this is due to the specific activity of alpha-secretase, we characterized mice overexpressing an inactive form of ADAM10 (ADAM10[E384A]; ADAM10-dn). T…

ADAM10Morris water navigation taskGlutamic AcidStimulationMice TransgenicADAM10 ProteinAmyloid beta-Protein PrecursorMiceIn vivoAlzheimer DiseaseDisintegrinReaction TimeAnimalsHumansIsoleucineProtein precursorMaze LearningSwimmingMetalloproteinaseAlaninebiologyBehavior AnimalChemistryGeneral NeuroscienceAge FactorsMembrane ProteinsValineGeneral MedicineCell biologyMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyADAM ProteinsDisease Models Animalbiology.proteinSpecific activityGeriatrics and GerontologyAmyloid Precursor Protein SecretasesJournal of Alzheimer's disease : JAD
researchProduct

Aequorin-expressing yeast emits light under electric control

2011

In this study, we show the use of direct external electrical stimulation of a jellyfish luminescent calcium-activated protein, aequorin, expressed in a transgenic yeast strain. Yeast cultures were electrically stimulated through two electrodes coupled to a standard power generator. Even low (1.5. V) electric pulses triggered a rapid light peak and serial light pulses were obtained after electric pulses were applied periodically, suggesting that the system is re-enacted after a short refraction time. These results open up a new scenario, in the very interphase between synthetic biology and cybernetics, in which complex cellular behavior might be subjected to electrical control.

Activated proteinsLightScyphozoaAequorinApplied Microbiology and BiotechnologyElectricityHydroxidesCellular behaviorsPriority journalYeast electro-stimulationbiologyPhosphorescencePower generatorsGeneral MedicineElectrostimulationMAQUINAS Y MOTORES TERMICOSElectrodeElectric pulseInterphaseBioluminescenceYeast cultureGenetic EngineeringMATEMATICA APLICADABiotechnologyPotassium CompoundsLight pulse generatorsSaccharomyces cerevisiaeBioengineeringNanotechnologyLight pulseSaccharomyces cerevisiaeElectrical stimulationsYeast strainArticleAequorinBioluminescenceBiologySynthetic biologyBioelectronicsBioelectronicsbiology.organism_classificationElectric controlYeastElectric StimulationYeastFISICA APLICADABiophysicsbiology.proteinProtein expressionJellyfishElectrical controlLuminescenceCell functionTransgenics
researchProduct

Coexpression of IL-6 and soluble IL-6R causes nodular regenerative hyperplasia and adenomas of the liver

1998

Studies with tumor necrosis factor p55 receptor- and interleukin-6 (IL-6)-deficient mice have shown that IL-6 is required for hepatocyte proliferation and reconstitution of the liver mass after partial hepatectomy. The biological activities of IL-6 are potentiated when this cytokine binds soluble forms of its specific receptor subunit (sIL-6R) and the resulting complex interacts with the transmembrane signaling chain gp130. We show here that double transgenic mice expressing high levels of both human IL-6 and sIL-6R under the control of liver-specific promoters spontaneously develop nodules of hepatocellular hyperplasia around periportal spaces and present signs of sustained hepatocyte prol…

AdenomaSTAT3 Transcription FactorAdenomail-6; liver adenomas; nodular hyperplasia; soluble il-6rMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-mycMiceMyeloproliferative Disordersil-6medicineAnimalsnodular hyperplasiaReceptorMolecular BiologyHyperplasialiver adenomasHaptoglobinsGeneral Immunology and MicrobiologyInterleukin-6General NeuroscienceLiver NeoplasmsHyperplasiaGlycoprotein 130medicine.diseaseReceptors Interleukin-6Liver regenerationLiver RegenerationDNA-Binding Proteinsmedicine.anatomical_structureGene Expression RegulationLiverSolubilityHepatocyteTrans-ActivatorsCancer researchEndothelium Vascularsoluble il-6rNodular regenerative hyperplasiaResearch ArticleThe EMBO Journal
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Coexpression of TGF-β1 and IL-10 Enables Regulatory T Cells to Completely Suppress Airway Hyperreactivity

2008

Abstract In allergic airway disease, Treg may play an important role in the modulation of airway hyperreactivity (AHR) and inflammation. We therefore investigated the therapeutic potential of Treg in an Ag-dependent murine asthma model. We here describe that AHR can be completely suppressed by adoptive transfer of Treg overexpressing active TGF-β1. Using mice with impaired TGF-β signaling in T cells, we could demonstrate that TGF-β signaling in recipient effector T cells or transferred Treg themselves is not required for the protective effects on AHR. However, the expression of IL-10 by Treg was found to be essential for the suppression of AHR, since Treg overexpressing active TGF-β1 but de…

Adoptive cell transferTransgeneImmunologyGene ExpressionMice Transgenicchemical and pharmacologic phenomenaInflammationT-Lymphocytes RegulatoryTransforming Growth Factor beta1MiceRespiratory HypersensitivitymedicineAnimalsImmunology and AllergyAsthmaInflammationbusiness.industryEffectorhemic and immune systemsrespiratory systemmedicine.diseaseAdoptive TransferAirway hyperreactivityInterleukin-10respiratory tract diseasesDisease Models AnimalInterleukin 10Immunologymedicine.symptombusinessSignal TransductionTransforming growth factorThe Journal of Immunology
researchProduct

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
researchProduct