Search results for "Cytometry"

showing 10 items of 852 documents

Extramedullary Expansion of Hematopoietic Progenitor Cells in Interleukin (IL)-6–sIL-6R Double Transgenic Mice

1997

Soluble cytokine receptors modulate the activity of their cognate ligands. Interleukin (IL)-6 in association with the soluble IL-6 receptor (sIL-6R) can activate cells expressing the gp130 signal transducer lacking the specific IL-6R. To investigate the function of the IL-6–sIL-6R complex in vivo and to discriminate the function of the IL-6–sIL-6R complex from the function of IL-6 alone, we have established a transgenic mouse model. Double-transgenic mice coexpressing IL-6 and sIL-6R were generated and compared with IL-6 and sIL-6R single-transgenic mice. The main phenotype found in IL-6–sIL-6R mice was a dramatic increase of extramedullary hematopoietic progenitor cells in liver and spleen…

Cellular differentiationmedicine.medical_treatmentImmunologyMice TransgenicCell SeparationBiologyArticleMiceAntigens CDCytokine Receptor gp130medicineAnimalsHumansImmunology and AllergyPeripheral blood cellInterleukin 6Interleukin 3Membrane GlycoproteinsInterleukin-6Body WeightInterleukinCell DifferentiationArticlesOrgan SizeFlow CytometryHematopoietic Stem CellsGlycoprotein 130ImmunohistochemistryMolecular biologyCell biologymedicine.anatomical_structureCytokineLiverbiology.proteinBone marrowCell DivisionSpleenSignal TransductionJournal of Experimental Medicine
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Leukocyte Redistribution: Effects of Beta Blockers in Patients with Chronic Heart Failure

2009

BACKGROUND:Overproduction of pro-inflammatory cytokines is a well established factor in the progression of chronic heart failure (CHF). Changes in cellular immunity have not been widely studied, and the impact of standard medication is uncertain. Here we investigate whether a leukocyte redistribution occurs in CHF and whether this effect is influenced by beta-blocker therapy. METHODOLOGY:We prospectively studied 75 patients with systolic CHF (age: 68+/-11 years, left ventricular ejection fraction 32+/-11%, New York Heart Association class 2.5+/-0.7) and 20 age-matched healthy control subjects (age: 63+/-10 years). We measured the response of cells to endotoxin exposure in vitro, analysed su…

Cellular immunityAdrenergic beta-AntagonistsCardiovascular Disorders/Heart Failurelcsh:MedicineVentricular Function LeftAdrenergic beta-AntagonistsLeukocytesHumansMedicineIn patientProspective Studiescardiovascular diseaseslcsh:ScienceProspective cohort studyAgedHeart FailureMultidisciplinaryVentricular functionbusiness.industrylcsh:RCase-control studyMiddle AgedFlow Cytometrymedicine.diseaseCase-Control StudiesImmunology/Leukocyte ActivationHeart failureImmunologylcsh:QbusinessImmunology/Leukocyte DevelopmentResearch ArticlePLoS ONE
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Circulating specific antibodies enhance systemic cross-priming by delivery of complexed antigen to dendritic cells in vivo

2012

Increasing evidence suggests that antibodies can have stimulatory effects on T-cell immunity. However, the contribution of circulating antigen-specific antibodies on MHC class I cross-priming in vivo has not been conclusively established. Here, we defined the role of circulating antibodies in cross-presentation of antigen to CD8(+) T cells. Mice with hapten-specific circulating antibodies, but naϊve for the T-cell antigen, were infused with haptenated antigen and CD8(+) T-cell induction was measured. Mice with circulating hapten-specific antibodies showed significantly enhanced cross-presentation of the injected antigen compared with mice that lacked these antibodies. The enhanced cross-pre…

Cellular immunityOvalbuminImmunologyMice Transgenicchemical and pharmacologic phenomenaAntigen-Antibody ComplexCD8-Positive T-LymphocytesBiologyDendritic cellsAntibodiesMiceCross-PrimingImmune systemAntigenAntigens NeoplasmMHC class ITcellsAnimalsImmunology and AllergyImmunity CellularB cellsCross-presentationHistocompatibility Antigens Class ICross-presentationSerum Albumin BovineFlow CytometryCD11c AntigenMice Inbred C57BLMacrophage-1 antigenHumoral immunityImmunologybiology.proteinAntibodyHaptensEuropean Journal of Immunology
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Reviewing the identity of the Maltese Polypodium (Polypodiaceae) – new evidence from morphology and flow cytometry

2020

The first record of Polypodium from Gozo (Maltese Islands) was described as a new endemic taxon, Polypodium vulgare subsp. melitense, based on its unique set of morphological characters. It was treated as a novelty and designated as a subspecies of P. vulgare mainly due to the lack of paraphyses, the presence of 10–16 annular cells, and a mean spore length of 64 μm. The fern was reassessed by us employing a more rigid morphological analysis and the application of flow cytometry. The absence of paraphyses was confirmed, but the number of annular cells (5–11) and the spore length (70–79 μm) differed from the previous study. These and other morphological traits, the phenology (leaf-shedding in…

Central Mediterranean Regionbiologymedicine.diagnostic_testSettore BIO/02 - Botanica SistematicaIdentity (social science)Morphology (biology)Plant ScienceFlora of Maltabiology.organism_classificationlanguage.human_languageNuclear DNA amountPolypodium vulgare subsp. melitenseFlow cytometryPolypodiumMaltesePolypodiaceaeEvolutionary biologySettore BIO/03 - Botanica Ambientale E ApplicataFernsmedicinelanguageParaphysesEcology Evolution Behavior and SystematicsNova Hedwigia
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T helper cell- and CD40-dependent germline IgM prevents chronic virus-induced demyelinating disease

2012

Generation of antiviral IgM is usually considered as a marker of a short-lived initial antibody response that is replaced by hypermutated and more-efficient IgG. However, once viruses have established a particular niche for their persistence (e.g., within the CNS), the immune system has to specifically mobilize a broad range of antimicrobial effectors to contain the pathogen in the long term. Infection of the CNS with the mouse hepatitis virus (MHV) provides a unique model situation in which the extent of inflammatory CNS disease is determined by the balance between antiviral immune control, viral replication, and immune-mediated damage. We show here that whereas antibody- or B cell-defici…

Central Nervous SystemEnzyme-Linked Immunospot AssayFluorescent Antibody TechniqueVirusMice03 medical and health sciences0302 clinical medicineImmune systemCytidine DeaminaseActivation-induced (cytidine) deaminaseDemyelinating diseasemedicineAnimalsCD40 Antigens030304 developmental biologyMice KnockoutAnalysis of VarianceB-LymphocytesMurine hepatitis virus0303 health sciencesMultidisciplinaryCD40biologyT-Lymphocytes Helper-InducerT helper cellBiological SciencesFlow Cytometrymedicine.diseaseVirology3. Good healthmedicine.anatomical_structureImmunoglobulin MViral replicationImmunologybiology.proteinAntibodyDemyelinating Diseases030215 immunologyProceedings of the National Academy of Sciences
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Cascades of transcriptional induction during dendritic cell maturation revealed by genome-wide expression analysis.

2003

Dendritic cells (DC) are central regulators of immunity. Signal-induced maturation of DCs is assumed to be the starting point for specific immune responses. To further understand this process, we analyzed the alteration of transcript profiles along the time course of CD40 ligand-induced maturation of human myeloid DCs by Affymetrix GeneChip microarrays covering >6800 genes. Besides rediscovery of genes already described as associated with DC maturation proving reliability of the methods used, we identified clusterin as novel maturation marker. Looking across the time course, we observed synchronized kinetics of distinct functional groups of molecules whose temporal coregulation underscores …

ChemokineTime FactorsMicroarrayTranscription GeneticCell Survivalmedicine.medical_treatmentImmunoglobulinsBiochemistryMiceAntigens CDGeneticsmedicineAnimalsHumansMolecular BiologyGeneCells CulturedOligonucleotide Array Sequence AnalysisMembrane GlycoproteinsClusterinbiologyGenome HumanReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingDendritic cell3T3 CellsDendritic CellsFlow CytometryMolecular biologyCell biologyGene expression profilingCytokinebiology.proteinB7-1 AntigenRNAB7-2 AntigenDNA microarrayBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

2004

In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity…

Chemokinemedicine.medical_treatmentPhagocytosisChemokine CXCL2ImmunologyHyphaeCell CountReceptors Cell SurfaceMicrobiologyMicrobiologyMicePhagocytosisIn vivoCandida albicansmedicineAnimalsMacrophageCandida albicansCells CulturedMice KnockoutToll-like receptorMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisFlow Cytometrybiology.organism_classificationImmunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLDisease Models AnimalInfectious DiseasesCytokineMacrophages Peritonealbiology.proteinChemokinesReactive Oxygen SpeciesMicrobes and Infection
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The Bile Acid Receptor GPBAR-1 (TGR5) Modulates Integrity of Intestinal Barrier and Immune Response to Experimental Colitis

2011

Background GP-BAR1, a member G protein coupled receptor superfamily, is a cell surface bile acid-activated receptor highly expressed in the ileum and colon. In monocytes, ligation of GP-BAR1 by secondary bile acids results in a cAMP-dependent attenuation of cytokine generation. Aims To investigate the role GP-BAR1 in regulating intestinal homeostasis and inflammation-driven immune dysfunction in rodent models of colitis. Methods Colitis was induced in wild type and GP-BAR1−/− mice by DSS and TNBS administration. Potential GP-BAR1 agonists were identified by in silico screening and computational docking studies. Results GP-BAR1−/− mice develop an abnormal morphology of colonic mucous cells a…

Cholera ToxinCD14Biophysicslcsh:MedicineInflammationGastroenterology and HepatologyBiologyLigandsBiochemistryPermeabilityReceptors G-Protein-CoupledTight JunctionsMiceCrohn DiseaseCiprofloxacinMolecular Cell BiologymedicineAnimalsUlcerative ColitisIntestinal MucosaProtein PrecursorsBiomacromolecule-Ligand InteractionsColitislcsh:ScienceReceptorBiologyMice KnockoutMultidisciplinaryIntestinal permeabilityHaptoglobinsPhysicsInflammatory Bowel Diseaselcsh:RImmunityZonulinColitisFlow Cytometrymedicine.diseaseMolecular biologyG protein-coupled bile acid receptorImmunologyTLR4Medicinelcsh:Qmedicine.symptomCytometryResearch ArticlePLoS ONE
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Dependence on nuclear factor of activated T-cells (NFAT) levels discriminates conventional T cells from Foxp3 + regulatory T cells

2012

Several lines of evidence suggest nuclear factor of activated T-cells (NFAT) to control regulatory T cells: thymus-derived naturally occurring regulatory T cells (nTreg) depend on calcium signals, the Foxp3 gene harbors several NFAT binding sites, and the Foxp3 (Fork head box P3) protein interacts with NFAT. Therefore, we investigated the impact of NFAT on Foxp3 expression. Indeed, the generation of peripherally induced Treg (iTreg) by TGF-β was highly dependent on NFAT expression because the ability of CD4 + T cells to differentiate into iTreg diminished markedly with the number of NFAT family members missing. It can be concluded that the expression of Foxp3 in TGF-β–induced iTreg depends…

Chromatin ImmunoprecipitationAdoptive cell transferT-LymphocytesImmunoblottingFluorescent Antibody TechniqueLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmune DiseasesProinflammatory cytokineMiceTransforming Growth Factor betaAnimalsHumansHomeodomain ProteinsMultidisciplinaryNFATC Transcription FactorsbiologyFOXP3Forkhead Transcription FactorsNFATTransforming growth factor betaBiological SciencesColitisFlow CytometryNFATC Transcription FactorsAdoptive TransferMolecular biologyCell biologyTransplantationCyclosporinebiology.proteinChromatin immunoprecipitationProceedings of the National Academy of Sciences
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EphrinB2 controls vessel pruning through STAT1-JNK3 signalling

2014

Angiogenesis produces primitive vascular networks that need pruning to yield hierarchically organized and functional vessels. Despite the critical importance of vessel pruning to vessel patterning and function, the mechanisms regulating this process are not clear. Here we show that EphrinB2, a well-known player in angiogenesis, is an essential regulator of endothelial cell death and vessel pruning. This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-terminal kinase 3 activity via STAT1. JNK3 activation causes endothelial cell death. In the absence of JNK3, hyaloid vessel physiological pruning is impaired, associated with abnormal persistence of hyaloid vessel…

Chromatin ImmunoprecipitationCell SurvivalAngiogenesisImmunoblottingRegulatorFluorescent Antibody TechniqueNeovascularization PhysiologicGeneral Physics and AstronomyEphrin-B2Persistent Hyperplastic Primary VitreousIn Vitro TechniquesBiologyBioinformaticsMicrophthalmiaArticleGeneral Biochemistry Genetics and Molecular BiologyNeovascularizationMiceMitogen-Activated Protein Kinase 10Human Umbilical Vein Endothelial CellsmedicineAnimalsHumansImmunoprecipitationInvolution (medicine)Pruning (decision trees)Cell ProliferationMice KnockoutMultidisciplinaryNeovascularization PathologicfungiEndothelial CellsRetinal VesselsGeneral ChemistryFlow Cytometrymedicine.diseaseCell biologyEndothelial stem cellSTAT1 Transcription Factornervous systemPersistent hyperplastic primary vitreousGene Knockdown Techniquescardiovascular systemmedicine.symptomSignal TransductionNature Communications
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