Search results for " Transgenic"

showing 10 items of 522 documents

Redirection of T cells by delivering a transgenic mouse-derived MDM2 tumor antigen-specific TCR and its humanized derivative is governed by the CD8 c…

1999

Retroviral transfer of T cell antigen receptor (TCR) genes selected by circumventing tolerance to broad tumor- and leukemia-associated antigens in human leukocyte antigen (HLA)-A*0201 (A2.1) transgenic (Tg) mice allows the therapeutic reprogramming of human T lymphocytes. Using a human CD8 x A2.1/Kb mouse derived TCR specific for natural peptide-A2.1 (pA2.1) complexes comprising residues 81-88 of the human homolog of the murine double-minute 2 oncoprotein, MDM2(81-88), we found that the heterodimeric CD8 alpha beta coreceptor, but not normally expressed homodimeric CD8 alpha alpha, is required for tetramer binding and functional redirection of TCR- transduced human T cells. CD8+T cells that…

CD4-Positive T-LymphocytesCD3T cellReceptors Antigen T-Cell alpha-betaImmunologyEpitopes T-LymphocyteMice TransgenicBiologyCD8-Positive T-LymphocytesEpitopeMiceAntigenCell Line TumorHLA-A2 AntigenmedicineCytotoxic T cellAnimalsHumansReverse Transcriptase Polymerase Chain ReactionT-cell receptorProto-Oncogene Proteins c-mdm2Flow CytometryVirologyMolecular biologyTumor antigenmedicine.anatomical_structureSelf Tolerancebiology.proteinCD8Immunologic research
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MHC class II-expressing hepatocytes function as antigen-presenting cells and activate specific CD4 T lymphocyutes.

2003

The ability to activate CD4 T cells is restricted to antigen-presenting cells that express major histocompatibility complex (MHC) class II molecules. Parenchymal cells normally do not express MHC class II molecules; however, in clinical hepatitis, viral or autoimmune, hepatocytes often exhibit aberrant MHC class II expression. It is not known whether MHC class II-expressing hepatocytes can function as antigen-presenting cells, but it has been suggested that aberrant MHC class II expression by parenchymal cells may cause autoimmune disease. Therefore, we generated transgenic mice that specifically overexpress class II transactivator molecules in hepatocytes. Hepatocytes from these mice exhib…

CD4-Positive T-LymphocytesCD74Antigen presentationCD1Antigen-Presenting CellsGene ExpressionMice Inbred StrainsMice TransgenicLymphocyte ActivationHepatitisMiceMHC class ICytotoxic T cellAnimalsMHC class IIHepatologybiologyAntigen processingHistocompatibility Antigens Class IINuclear ProteinsMHC restrictionCell biologyImmunologybiology.proteinHepatocytesTrans-ActivatorsHepatology (Baltimore, Md.)
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A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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Cross-recognition of a myelin peptide by CD8+ T cells in the CNS is not sufficient to promote neuronal damage.

2015

Multiple sclerosis (MS) is an inflammatory disease of the CNS thought to be driven by CNS-specific T lymphocytes. Although CD8+T cells are frequently found in multiple sclerosis lesions, their distinct role remains controversial because direct signs of cytotoxicity have not been confirmedin vivo. In the present work, we determined that murine ovalbumin-transgenic (OT-1) CD8+T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40–54 (MOG40–54) bothin vitroandin vivo. The aim of this study was to investigate whether such cross-recognizing CD8+T cells are capable of inducing CNS damagein vivo. Using intravital two-photon microscopy in the mouse model of multiple sclerosis, …

CD4-Positive T-LymphocytesCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisAutoimmunityMice TransgenicCD8-Positive T-Lymphocytesmedicine.disease_causeMyelin oligodendrocyte glycoproteinMyelinMiceIn vivomedicineCytotoxic T cellAnimalsCells CulturedCell ProliferationbiologyCell DeathGeneral NeuroscienceMultiple sclerosisArticlesmedicine.diseaseMolecular mimicrymedicine.anatomical_structureImmunologyNerve Degenerationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinCD8Intravital microscopyThe Journal of neuroscience : the official journal of the Society for Neuroscience
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Regulatory T Cells Accumulate and Proliferate in the Ischemic Hemisphere for up to 30 Days after MCAO

2012

Local and peripheral immune responses are activated after ischemic stroke. In our present study, we investigated the temporal distribution, location, induction, and function of regulatory T cells (Tregs) and the possible involvement of microglia, macrophages, and dendritic cells after middle cerebral artery occlusion (MCAO). C57BL/6J and Foxp3EGFP transgenic mice were subjected to 30 minutes MCAO. On days 7, 14, and 30 after MCAO, Tregs and antigen presenting cells were analyzed using fluorescence activated cell sorting multicolor staining and immunohistochemistry. A strong accumulation of Tregs was observed on days 14 and 30 in the ischemic hemisphere accompanied by the elevated presence …

CD4-Positive T-LymphocytesGenetically modified mousePathologymedicine.medical_specialtyTime FactorsAntigen-Presenting CellsMice Transgenicchemical and pharmacologic phenomenaLymphocyte ActivationT-Lymphocytes RegulatoryNeuroprotectionFlow cytometryMice03 medical and health sciences0302 clinical medicineImmune systemGenes ReportermedicineAnimalsLymphocyte CountIL-2 receptorAntigen-presenting cellCell Proliferation030304 developmental biologyHomeodomain Proteins0303 health sciencesmedicine.diagnostic_testMicrogliabusiness.industryInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription FactorsInfarction Middle Cerebral Arteryhemic and immune systemsFlow CytometryImmunohistochemistryMice Inbred C57BLmedicine.anatomical_structureNeurology030220 oncology & carcinogenesisImmunologyOriginal ArticleNeurology (clinical)CorrigendumCardiology and Cardiovascular Medicinebusiness030217 neurology & neurosurgeryJournal of Cerebral Blood Flow & Metabolism
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Molecular Basis for the Interaction of the Hepatitis B Virus Core Antigen with the Surface Immunoglobulin Receptor on Naive B Cells

2001

ABSTRACTThe nucleocapsid of the hepatitis B virus (HBV) is composed of 180 to 240 copies of the HBV core (HBc) protein. HBc antigen (HBcAg) capsids are extremely immunogenic and can activate naive B cells by cross-linking their surface receptors. The molecular basis for the interaction between HBcAg and naive B cells is not known. The functionality of this activation was evidenced in that low concentrations of HBcAg, but not the nonparticulate homologue HBV envelope antigen (HBeAg), could prime naive B cells to produce anti-HBc in vitro with splenocytes from HBcAg- and HBeAg-specific T-cell receptor transgenic mice. The frequency of these HBcAg-binding B cells was estimated by both hybridom…

CD4-Positive T-LymphocytesImmunologyNaive B cellAntigen presentationMolecular Sequence DataImmunoglobulin Variable RegionMice Transgenicmedicine.disease_causeAntibodies ViralMicrobiologyMiceAntigenVirologymedicineAnimalsHumansAmino Acid SequenceReceptors ImmunologicHepatitis B virusAntigen PresentationB-LymphocytesMice Inbred BALB Cbiologyvirus diseasesAntibodies MonoclonalVirologyMolecular biologyHepatitis B Core Antigensdigestive system diseasesPeptide FragmentsVirus-Cell InteractionsHBcAgHBeAgImmunoglobulin MImmunoglobulin MInsect Sciencebiology.proteinMice Inbred CBAImmunoglobulin Light ChainsBinding Sites AntibodyAntibodyImmunoglobulin Heavy ChainsSequence Alignment
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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Inhibitors of β-catenin affect the immuno-phenotype and functions of dendritic cells in an inhibitor-specific manner

2015

Many tumors are characterized by mutation-induced constitutive activation of β-catenin which promotes tumor growth and survival. Consequently, the development of specific β-catenin inhibitors for tumor therapy has come into the focus of drug development. β-Catenin was also shown to contribute to the tolerance-promoting function of unstimulated dendritic cells (DCs). In response to activation, DCs acquire potent T cell stimulatory capacity and induce profound tumor antigen-specific immune responses. Here we asked for effects of pre-clinically established β-catenin inhibitors (CCT-031374, iCRT-5, PNU-75654) on mouse bone marrow-derived (BM)DCs. All three inhibitors moderately increased surfac…

CD4-Positive T-LymphocytesLipopolysaccharides0301 basic medicineCell SurvivalOvalbuminT cellImmunologyPopulationAntineoplastic AgentsBone Marrow CellsMice Transgenicchemical and pharmacologic phenomena03 medical and health sciencesImmune systemmedicineAnimalsImmunology and AllergyeducationCells Culturedbeta CateninCell ProliferationPharmacologyCD86education.field_of_studyCD40biologyFollicular dendritic cellsCell growthhemic and immune systemsDendritic CellsCell biologyMice Inbred C57BLPhenotype030104 developmental biologymedicine.anatomical_structurebiology.proteinCytokinesCD80International Immunopharmacology
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Glycoprotein 96-activated dendritic cells induce a CD8-biased T cell response.

2005

Heat shock proteins (Hsps) are able to induce protective immune responses against pathogens and tumors after injection into immunocompetent hosts. The activation of components of the adaptive immune system, including cytotoxic T lymphocytes specific for pathogen- or tumor-derived peptides, is crucial for the establishment of immuno- protection. Hsps acquire these peptides during intracellular protein degradation and when released during necrotic cell death, facilitate their uptake and Minor Histocompatibility Complex (MHC)-restricted representation by professional antigen-presenting cells (APCs). In addition, the interaction of Hsps with APCs, including the Endoplasmatic Reticulum (ER)-resi…

CD4-Positive T-LymphocytesLipopolysaccharidesAntigen-Presenting CellsBone Marrow CellsMice TransgenicReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexLymphocyte ActivationBiochemistryMiceImmune systemHeat shock proteinCytotoxic T cellAnimalsHumansAntigen-presenting cellCells CulturedMembrane GlycoproteinsToll-Like ReceptorsCell DifferentiationCell BiologyDendritic cellDendritic CellsOriginal ArticlesAcquired immune systemLymphocyte SubsetsCell biologyMice Inbred C57BLToll-Like Receptor 4biology.proteinInflammation MediatorsCD8Signal TransductionCell stresschaperones
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Defective T helper response of hepatocyte-stimulated CD4 T cells impairs antiviral CD8 response and viral clearance.

2007

Background & Aims: In hepatitis, hepatocytes gain the ability to express major histocompatibility complex (MHC) class II molecules and to present antigen to CD4 T cells. Here, we investigated whether MHC class II-expressing hepatocytes influence in vitro the differentiation of CD4 T cells and in vivo the T-cell response to and control of viral infection. Methods: Class II transactivator-transgenic hepatocytes that constitutively express MHC class II molecules were used to stimulate CD4 T cells in vitro, and the effector response type of the stimulated CD4 T cells was determined. The in vivo relevance of the obtained findings was confirmed by infecting nontransgenic or class II transactivato…

CD4-Positive T-LymphocytesMHC class IIHepatologybiologyCD8 AntigensGastroenterologyCD1Mice TransgenicT helper cellT-Lymphocytes Helper-InducerMHC restrictionCD8-Positive T-LymphocytesMicemedicine.anatomical_structureMHC class IImmunologyCD4 Antigensbiology.proteinmedicineHepatocytesCytotoxic T cellAnimalsAntigen-presenting cellCD8Gastroenterology
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