Search results for "Transgenic"

showing 10 items of 552 documents

Microglial activation milieu controls regulatory T cell responses.

2013

Abstract Although mechanisms leading to brain-specific inflammation and T cell activation have been widely investigated, regulatory mechanisms of local innate immune cells in the brain are only poorly understood. In this study, to our knowledge we show for the first time that MHC class II+CD40dimCD86dimIL-10+ microglia are potent inducers of Ag-specific CD4+Foxp3+ regulatory T cells (Tregs) in vitro. Microglia differentially regulated MHC class II expression, costimulatory molecules, and IL-10 depending on the amount of IFN-γ challenge and Ag dose, promoting either effector T cell or Treg induction. Microglia-induced Tregs were functionally active in vitro by inhibiting Ag-specific prolifer…

Encephalomyelitis Autoimmune ExperimentalRegulatory T cellT cellImmunologychemical and pharmacologic phenomenaMice TransgenicLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterferon-gammaMiceImmune systemT-Lymphocyte SubsetsmedicineImmune ToleranceImmunology and AllergyAnimalsCells CulturedCD86MHC class IIbiologyMicrogliaHistocompatibility Antigens Class IIFOXP3Brainhemic and immune systemsForkhead Transcription FactorsCoculture TechniquesCell biologyInterleukin-10Mice Inbred C57BLmedicine.anatomical_structureCellular Microenvironmentbiology.proteinMicrogliaJournal of immunology (Baltimore, Md. : 1950)
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IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice

2009

The clear association of Th17 cells with autoimmune pathogenicity implicates Th17 cytokines as critical mediators of chronic autoimmune diseases such as EAE. To study the impact of IL-17A on CNS inflammation, we generated transgenic mice in which high levels of expression of IL-17A could be initiated after Cre-mediated recombination. Although ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell–specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice. In the context of EAE, neither the T cell–driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease. Sin…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentT cellEncephalomyelitisPopulation610 Medicine & healthMice TransgenicInflammation2700 General Medicine10263 Institute of Experimental ImmunologyMyelin oligodendrocyte glycoproteinMicemedicineAnimalseducationCells CulturedGlycoproteinseducation.field_of_studybiologybusiness.industryInterleukin-17General MedicineTh1 Cellsmedicine.diseasePeptide FragmentsMice Inbred C57BLCytokinemedicine.anatomical_structureImmunologybiology.protein570 Life sciences; biologyExperimental pathologyFemaleMyelin-Oligodendrocyte GlycoproteinInterleukin 17medicine.symptombusinessGranulocytesResearch Article
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Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

2006

Endothelin (ET-1) has been shown to crucially contribute to UV-induced skin responses such as tanning. To test whether ET-1 is also involved in early cutaneous reactions to UV, we assessed ET-1 skin levels in UV-irradiated mice. In correlation with the levels of UV-induced skin inflammation, ET-1 concentrations increased substantially and continually. Moreover, blocking of ET-1 receptors (ET A ) resulted in significantly decreased cutaneous inflammation following UV irradiation. When we assessed skin responses to ET-1 injections, we observed prominent mast cell degranulation and mast cell-dependent inflammation. Since mast cells also critically contributed to UV-induced inflammation, we det…

Endothelin A Receptor AntagonistsUltraviolet RaysCell DegranulationRatónDermatitisMice TransgenicInflammationBiologyPharmacologyCell DegranulationPathology and Forensic MedicineMicemedicineAnimalsMast CellsReceptorInflammationEndothelin-1integumentary systemDegranulationDose-Response Relationship RadiationReceptor Endothelin AMast cellEndothelin 1medicine.anatomical_structureImmunologymedicine.symptomEndothelin receptorRegular ArticlesThe American Journal of Pathology
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Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells

2010

Glioblastoma is a highly angiogenetic malignancy, the neoformed vessels of which are thought to arise by sprouting of pre-existing brain capillaries. The recent demonstration that a population of glioblastoma stem-like cells (GSCs) maintains glioblastomas indicates that the progeny of these cells may not be confined to the neural lineage. Normal neural stem cells are able to differentiate into functional endothelial cells. The connection between neural stem cells and the endothelial compartment seems to be critical in glioblastoma, where cancer stem cells closely interact with the vascular niche and promote angiogenesis through the release of vascular endothelial growth factor(VEGF) and str…

EndotheliumAngiogenesisTransplantation HeterologousSettore MED/27 - NEUROCHIRURGIAMice TransgenicMice SCIDBiologyModels BiologicalMiceVasculogenesisNeural Stem CellsMice Inbred NODCell Line TumormedicineAnimalsHumansCell LineageVasculogenic mimicryglioblastoma tumor vascularizationIn Situ Hybridization FluorescenceChromosome AberrationsMultidisciplinaryNeovascularization PathologicEndothelial CellsCell DifferentiationVascular endothelial growth factor BEndothelial stem cellVascular endothelial growth factor Amedicine.anatomical_structureVascular endothelial growth factor CTumor Markers BiologicalImmunologyCancer researchEndothelium VascularGlioblastomaNeoplasm TransplantationNature
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Lymphatic endothelial progenitors bud from the cardinal vein and intersomitic vessels in mammalian embryos.

2012

Abstract The lymphatic vasculature preserves tissue fluid balance by absorbing fluid and macromolecules and transporting them to the blood vessels for circulation. The stepwise process leading to the formation of the mammalian lymphatic vasculature starts by the expression of the gene Prox1 in a subpopulation of blood endothelial cells (BECs) on the cardinal vein (CV) at approximately E9.5. These Prox1-expressing lymphatic endothelial cells (LECs) will exit the CV to form lymph sacs, primitive structures from which the entire lymphatic network is derived. Until now, no conclusive information was available regarding the cellular processes by which these LEC progenitors exit the CV without co…

EndotheliumMesenchymegovernment.form_of_governmentRecombinant Fusion ProteinsImmunologyEmbryonic DevelopmentMice TransgenicBiologyBiochemistryMiceMicroscopy Electron TransmissionCell MovementVascular BiologymedicineAnimalsLymph sacsProgenitor cellEmbryonic Stem CellsHomeodomain ProteinsMice KnockoutBuddingMembrane GlycoproteinsCommon cardinal veinsTumor Suppressor ProteinsfungiCell BiologyHematologyAnatomyAdherens JunctionsCadherinsEmbryo MammalianCoronary VesselsCell biologyPlatelet Endothelial Cell Adhesion Molecule-1Lymphatic Endotheliummedicine.anatomical_structureLymphatic systemgovernmentsense organsEndothelium LymphaticBlood
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TGF-beta regulates airway responses via T cells.

2003

Abstract Allergic asthma is characterized by airway hyperreactivity, inflammation, and a Th2-type cytokine profile favoring IgE production. Beneficial effects of TGF-β and conflicting results regarding the role of Th1 cytokines have been reported from murine asthma models. In this study, we examined the T cell as a target cell of TGF-β-mediated immune regulation in a mouse model of asthma. We demonstrate that impairment of TGF-β signaling in T cells of transgenic mice expressing a dominant-negative TGF-β type II receptor leads to a decrease in airway reactivity in a non-Ag-dependent model. Increased serum levels of IFN-γ can be detected in these animals. In contrast, after injection of OVA …

Epitopes T-LymphocyteNitric Oxide Synthase Type IIImmunoglobulin EMiceAntibody SpecificityCell MovementT-Lymphocyte SubsetsTransforming Growth Factor betaImmunology and AllergyInterferon gammaLungInterleukin-13biologymedicine.diagnostic_testrespiratory systemImmunohistochemistrymedicine.anatomical_structureInterleukin 13Alum Compoundsmedicine.symptomBronchial HyperreactivityBronchoalveolar Lavage Fluidmedicine.drugGenetically modified mousemedicine.medical_specialtyOvalbuminT cellImmunologyCD2 AntigensInflammationMice Inbred StrainsMice TransgenicProtein Serine-Threonine KinasesInterferon-gammaInternal medicineAdministration InhalationmedicineAnimalsHumansAerosolsInflammationbusiness.industryReceptor Transforming Growth Factor-beta Type IITransforming growth factor betaImmunoglobulin ETh1 Cellsrespiratory tract diseasesEndocrinologyBronchoalveolar lavageImmunologybiology.proteinNitric Oxide SynthasebusinessReceptors Transforming Growth Factor betaJournal of immunology (Baltimore, Md. : 1950)
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Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
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Plasma clearance of human low-density lipoprotein in human apolipoprotein B transgenic mice is related to particle diameter.

2004

To test for intrinsic differences in metabolic properties of low-density lipoprotein (LDL) as a function of particle size, we examined the kinetic behavior of 6 human LDL fractions ranging in size from 251 to 265 A injected intravenously into human apolipoprotein (apo) B transgenic mice. A multicompartmental model was formulated and fitted to the data by standard nonlinear regression using the Simulation, Analysis and Modeling (SAAM II) program. Smaller sized LDL particles (251 to 257 A) demonstrated a significantly slower fractional catabolic rate (FCR) (0.050 +/- 0.045 h(-1)) compared with particles of larger size (262 to 265 A) (0.134 +/- -0.015 h(-1), P.03), and there was a significant …

Genetically modified mouseAdultMalemedicine.medical_specialtySimvastatinApolipoprotein BMetabolic Clearance RateEndocrinology Diabetes and MetabolismPlasma clearance low-density lipoprotein apolipoprotein B trangenic miceMice Transgenicchemistry.chemical_compoundMiceEndocrinologyInternal medicineBlood plasmamedicineAnimalsHumansParticle SizeApolipoproteins BPravastatinbiologyCatabolismMiddle AgedLipoproteins LDLEndocrinologychemistryLow-density lipoproteinModels Animalbiology.proteinRegression Analysislipids (amino acids peptides and proteins)Particle sizeNonlinear regressionLipoproteinMetabolism: clinical and experimental
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T Cell-Specific Overexpression of TGFß1 Fails to Influence Atherosclerosis in ApoE-Deficient Mice

2013

Clinical data have indicated a negative correlation between plasma TGFß1 concentrations and the extent of atherosclerosis and have thus led to the hypothesis that the pleiotropic cytokine may have anti-atherogenic properties. T-cells are currently discussed to significantly participate in atherogenesis, but the precise role of adaptive immunity in atherogenesis remains to be elucidated. TGFß1 is known to strongly modulate the function of T-cells, however, inhibition of TGFß1 signalling in T-cells of atherosclerosis-prone knock-out mice failed to unequivocally clarify the role of the cytokine for the development of atherosclerosis. In the present study, we thus tried to specify the role of T…

Genetically modified mouseApolipoprotein ELipoproteinsT-LymphocytesScienceCD3medicine.medical_treatmentT cellTransgeneMutantGene ExpressionMice TransgenicBiologyTransforming Growth Factor beta1MiceApolipoproteins EmedicineAnimalsHumansMultidisciplinaryQRAtherosclerosisAcquired immune systemCytokinemedicine.anatomical_structureImmunologyDisease Progressionbiology.proteinMedicineFemaleResearch ArticlePLoS ONE
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No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice

2008

summaryThe association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE-/-) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR-/-) may represent a better model of atherogenesis compared to ApoE-/- animals, we undertook experiments…

Genetically modified mouseApolipoprotein ETime FactorsGenotypeLipoproteinsTransgeneMice TransgenicBiologyLesionMicemedicineAnimalsHumansComplement ActivationAortaCrosses GeneticMice KnockoutC-reactive proteinAcute-phase proteinHematologyAtherosclerosisDietary FatsLipidsDisease Models AnimalC-Reactive ProteinPhenotypeReceptors LDLImmunologyLDL receptorKnockout mousebiology.proteinlipids (amino acids peptides and proteins)medicine.symptomThrombosis and Haemostasis
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