Search results for " Transgenic"

showing 10 items of 522 documents

Dendritic cell-derived IL-12p40 homodimer contributes to susceptibility in cutaneous leishmaniasis in BALB/c mice

2007

Abstract Protection against Leishmania major in resistant C57BL/6 mice is mediated by Th1 cells, whereas susceptibility in BALB/c mice is the result of Th2 development. IL-12 release by L. major-infected dendritic cells (DC) is critically involved in differentiation of Th1 cells. Previously, we reported that strain differences in the production of DC-derived factors, e.g., IL-1αβ, are in part responsible for disparate disease outcome. In the present study, we analyzed the release of IL-12 from DC in more detail. Stimulated DC from C57BL/6 and BALB/c mice released comparable amounts of IL-12p40 and p70. In the absence of IL-4, BALB/c DC produced significantly more IL-12p40 than C57BL/6 DC. D…

TransgeneImmunologyLeishmaniasis CutaneousMice TransgenicBiologyBALB/cMiceWestern blotSpecies SpecificityIn vivoImmunitymedicineImmunology and AllergyAnimalsLeishmania majorGenetic Predisposition to DiseaseCells CulturedLeishmania majorMice Inbred BALB Cmedicine.diagnostic_testInterleukin-12 Subunit p40Dendritic cellDendritic Cellsbiology.organism_classificationMolecular biologyInterleukin-12In vitroImmunity InnateMice Inbred C57BLImmunologyInterleukin-4DimerizationSignal Transduction
researchProduct

Differential Roles of Macrophages in Diverse Phases of Skin Repair

2010

Abstract Influx of macrophages plays a crucial role in tissue repair. However, the precise function of macrophages during the healing response has remained a subject of debate due to their functional dichotomy as effectors of both tissue injury and repair. We tested the hypothesis that macrophages recruited during the diverse phases of skin repair after mechanical injury exert specific functions to restore tissue integrity. For this purpose, we developed a mouse model that allows conditional depletion of macrophages during the sequential stages of the repair response. Depletion of macrophages restricted to the early stage of the repair response (inflammatory phase) significantly reduced the…

TransgeneImmunologyMice TransgenicCell SeparationBiologyFlow cytometryMiceSkin Physiological PhenomenamedicineAnimalsImmunology and AllergySkinSkin repairWound HealingSkin Physiological Phenomenamedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionEffectorMacrophagesGranulation tissueFlow CytometryImmunohistochemistryCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunologyImmunohistochemistryFunction (biology)The Journal of Immunology
researchProduct

Regulatory T Cells More Effectively Suppress Th1-Induced Airway Inflammation Compared with Th2

2011

Abstract Asthma is a syndrome with different inflammatory phenotypes. Animal models have shown that, after sensitization and allergen challenge, Th2 and Th1 cells contribute to the development of allergic airway disease. We have previously demonstrated that naturally occurring regulatory T cells (nTregs) can only marginally suppress Th2-induced airway inflammation and airway hyperresponsiveness. In this study, we investigated nTreg-mediated suppression of Th2-induced and Th1-induced acute allergic airway disease. We demonstrate in vivo that nTregs exert their suppressive potency via cAMP transfer on Th2- and Th1-induced airway disease. A comparison of both phenotypes revealed that, despite …

TransgeneImmunologyMice TransgenicInflammationT-Lymphocytes RegulatoryMiceTh2 CellsIn vivoImmunitymedicineAnimalsImmunology and AllergyPotencyCells CulturedSensitizationAsthmaInflammationMice KnockoutMice Inbred BALB Cbusiness.industryTh1 Cellsrespiratory systemmedicine.diseasePhenotypeCoculture TechniquesImmunity Innaterespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureAcute DiseaseImmunologyFemaleDisease SusceptibilityBronchial Hyperreactivitymedicine.symptombusinessThe Journal of Immunology
researchProduct

Insensitivity to Aβ42-lowering Nonsteroidal Anti-inflammatory Drugs and γ-Secretase Inhibitors Is Common among Aggressive Presenilin-1 Mutations

2007

Abeta42-lowering nonsteroidal anti-inflammatory drugs (NSAIDs) constitute the founding members of a new class of gamma-secretase modulators that avoid side effects of pan-gamma-secretase inhibitors on NOTCH processing and function, holding promise as potential disease-modifying agents for Alzheimer disease (AD). These modulators are active in cell-free gamma-secretase assays indicating that they directly target the gamma-secretase complex. Additional support for this hypothesis was provided by the observation that certain mutations in presenilin-1 (PS1) associated with early-onset familial AD (FAD) change the cellular drug response to Abeta42-lowering NSAIDs. Of particular interest is the P…

TransgeneMolecular Sequence DataMutantMice TransgenicCHO CellsBiologyPharmacologymedicine.disease_causeBiochemistryPresenilinMiceExonCricetulusAlzheimer DiseaseIn vivoCricetinaePresenilin-1medicineAnimalsHumansAmino Acid SequenceEnzyme InhibitorsMolecular BiologyMutationAmyloid beta-PeptidesSequence Homology Amino AcidDrug discoveryAnti-Inflammatory Agents Non-SteroidalCell BiologyPeptide FragmentsMutationbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseJournal of Biological Chemistry
researchProduct

Helicobacter pylori gamma-glutamyl transpeptidase and vacuolating cytotoxin promote gastric persistence and immune tolerance

2013

Infection with the gastric bacterial pathogen Helicobacter pylori is typically contracted in early childhood and often persists for decades. The immunomodulatory properties of H. pylori that allow it to colonize humans persistently are believed to also account for H. pylori ’s protective effects against allergic and chronic inflammatory diseases. H. pylori infection efficiently reprograms dendritic cells (DCs) toward a tolerogenic phenotype and induces regulatory T cells (Tregs) with highly suppressive activity in models of allergen-induced asthma. We show here that two H. pylori virulence determinants, the γ-glutamyl transpeptidase GGT and the vacuolating cytotoxin VacA, contribute critic…

TransgeneVirulenceMice Transgenicbacterial virulence factorspersistence strategieshygiene hypothesisMicrobiologyImmune toleranceMice03 medical and health sciences0302 clinical medicineBacterial ProteinsIn vivoImmune ToleranceAnimalsGamma-glutamyltransferasehuman microbiotaPathogen030304 developmental biology0303 health sciences1000 MultidisciplinaryMultidisciplinaryHelicobacter pyloribiologyStomach10061 Institute of Molecular Cancer Researchgamma-GlutamyltransferaseBiological SciencesHelicobacter pyloribiology.organism_classificationbacterial infections and mycosesCoculture TechniquesIn vitrodigestive system diseases3. Good healthMice Inbred C57BLImmunologybiology.protein570 Life sciences; biology030211 gastroenterology & hepatologypersistent bacterial infection
researchProduct

Naturally occurring short splice variant of CYLD positively regulates dendritic cell function

2009

Abstract Deubiquitination of NF-κB members by CYLD is crucial in controlling the magnitude and nature of cell activation. The role of the naturally occurring CYLD splice variant in dendritic cell (DC) function was analyzed using CYLDex7/8 mice, which lack the full-length CYLD (flCYLD) transcript and overexpress the short splice variant (sCYLD). Bone marrow–derived DCs from CYLDex7/8 mice display a hyperactive phenotype in vitro and in vivo and have a defect in establishing tolerance with the use of DEC-205–mediated antigen targeting to resting DCs. The combination of sCYLD overexpression and lack of flCYLD in CYLDex7/8 DCs leads to enhanced NF-κB activity accompanied by an increased nuclear…

Tumor suppressor geneTransgeneImmunologyRegulatorMice TransgenicBiologyBiochemistryDeubiquitinating Enzyme CYLDMiceAnimalsAntigen-presenting cellNF-kappa BDendritic CellsCell BiologyHematologyDendritic cellDeubiquitinating Enzyme CYLDCell biologyMice Inbred C57BLAlternative SplicingCysteine EndopeptidasesPhenotypeImmunologySignal transductionCell activationSignal TransductionBlood
researchProduct

Liver specific overexpression of platelet-derived growth factor-B accelerates liver cancer development in chemically induced liver carcinogenesis

2010

A genetic basis of hepatocellular carcinoma (HCC) has been well-established and major signaling pathways, such as p53, Wnt-signaling, transforming growth factor-β (TGF-β) and Ras pathways, have been identified to be essential to HCC development. Lately, the family of platelet-derived growth factors (PDGFs) has shifted to the center of interest. We have reported on spontaneously developing liver fibrosis in PDGF-B transgenic mice. Since HCC rarely occurs in healthy liver, but dramatically increases at the cirrhosis stage of which liver fibrosis is a preliminary stage, we investigated liver cancer development in chemically induced liver carcinogenesis in these mice. HCC induction was performe…

Vascular Endothelial Growth Factor AAlkylating AgentsCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularCirrhosisPlatelet-derived growth factorBlotting WesternMice TransgenicBiologymedicine.disease_causeImmunoenzyme TechniquesMicechemistry.chemical_compoundLiver Neoplasms ExperimentalInternal medicinemedicineAnimalsHumansDiethylnitrosamineRNA MessengerReverse Transcriptase Polymerase Chain ReactionCancerProto-Oncogene Proteins c-sismedicine.diseaseFibroblast Growth FactorsPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factorEndocrinologyOncologychemistryPhenobarbitalbiology.proteinAnticonvulsantsCarcinogenesisLiver cancerPlatelet-derived growth factor receptorTransforming growth factorInternational Journal of Cancer
researchProduct

VEGF receptor signaling links inflammation and tumorigenesis in colitis-associated cancer.

2010

Inflammation drives expression of VEGFR2, which is expressed on and drives growth of tumor cells in colitis-associated cancer.

Vascular Endothelial Growth Factor AColorectal cancerGene Expressionmedicine.disease_causechemistry.chemical_compoundMice0302 clinical medicineImmunology and AllergyDecoy receptorsCells CulturedMice Knockout0303 health sciencesMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionDextran Sulfaterespiratory systemColitisImmunohistochemistry3. Good healthUp-RegulationVascular endothelial growth factorVascular endothelial growth factor A030220 oncology & carcinogenesisColonic Neoplasmscardiovascular systemcirculatory and respiratory physiologySignal TransductionSTAT3 Transcription FactorImmunologyBlotting WesternMice TransgenicBiologyArticle03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyCell ProliferationVascular Endothelial Growth Factor Receptor-1CancerEndothelial CellsKinase insert domain receptorEpithelial CellsCell Biologymedicine.diseaseInflammatory Bowel DiseasesVascular Endothelial Growth Factor Receptor-2Mice Inbred C57BLHIF1AchemistryCancer researchCarcinogenesis030215 immunologyThe Journal of experimental medicine
researchProduct

Integrin-dependent and -independent functions of astrocytic fibronectin in retinal angiogenesis

2011

Fibronectin (FN) is a major component of the extracellular matrix and functions in cell adhesion, cell spreading and cell migration. In the retina, FN is transiently expressed and assembled on astrocytes (ACs), which guide sprouting tip cells and deposit a provisional matrix for sprouting angiogenesis. The precise function of FN in retinal angiogenesis is largely unknown. Using genetic tools, we show that astrocytes are the major source of cellular FN during angiogenesis in the mouse retina. Deletion of astrocytic FN reduces radial endothelial migration during vascular plexus formation in a gene dose-dependent manner. This effect correlates with reduced VEGF receptor 2 and PI3K/AKT signalli…

Vascular Endothelial Growth Factor AIntegrinsAngiogenesisIntegrinNeovascularization PhysiologicMice TransgenicExtracellular matrixMicePhosphatidylinositol 3-KinasesCell MovementAnimalsProtein Interaction Domains and MotifsMolecular BiologyResearch ArticlesMice KnockoutSprouting angiogenesisbiologyRetinal VesselsCell migrationKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Extracellular MatrixFibronectinsCell biologyMice Inbred C57BLFibronectinVascular endothelial growth factor AAstrocytesbiology.proteinHeparitin SulfateOligopeptidesProto-Oncogene Proteins c-aktIntegrin alpha5beta1Signal TransductionDevelopmental BiologyDevelopment
researchProduct

Tbx1 regulates Vegfr3 and is required for lymphatic vessel development

2010

Defects in lymphangiogenesis are added to the broad clinical manifestations of DiGeorge syndrome, caused by deletion of the T box transcription factor Tbx1.

Vascular Endothelial Growth Factor ATBX1Cellular differentiationBiologyMice03 medical and health sciences0302 clinical medicinestomatognathic systemReportLymphatic vesselmedicineAnimalsHumansLymphangiogenesisEnhancerCells CulturedResearch ArticlesLymphatic Vessels030304 developmental biology0303 health sciencesABNORMAL CAROTID ARTERIES; TRANSGENIC MICE; VELOCARDIOFACIAL SYNDROME; CARDIOVASCULAR DEFECTS; LYMPHANGIOGENESIS; LYMPHEDEMA; MOUSE; RECEPTOR-3; MUTATION; SYSTEMEndothelial CellsGene Expression Regulation DevelopmentalCell DifferentiationCell BiologyEmbryo Mammalian3. Good healthLymphangiogenesisCell biologyVascular endothelial growth factor ALymphatic systemmedicine.anatomical_structureVascular endothelial growth factor Cembryonic structuresImmunologyT-Box Domain Proteins030217 neurology & neurosurgeryJournal of Cell Biology
researchProduct