Search results for "Cytometry"

showing 10 items of 852 documents

Dendritic cells trigger tumor cell death by a nitric oxide-dependent mechanism.

2007

Abstract Dendritic cells (DCs) are well known for their capacity to induce adaptive antitumor immune response through Ag presentation and tumor-specific T cell activation. Recent findings reveal that besides this role, DCs may display additional antitumor effects. In this study, we provide evidence that LPS- or IFN-γ-activated rat bone marrow-derived dendritic cells (BMDCs) display killing properties against tumor cells. These cytotoxic BMDCs exhibit a mature DC phenotype, produce high amounts of IL-12, IL-6, and TNF-α, and retain their phagocytic properties. BMDC-mediated tumor cell killing requires cell-cell contact and depends on NO production, but not on perforin/granzyme or on death re…

Cytotoxicity ImmunologicLipopolysaccharidesT cellImmunologyBlotting WesternBone Marrow CellsBiologyNitric OxideImmune systemAdjuvants ImmunologicCell Line TumorNeoplasmsmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansFollicular dendritic cellsCell DeathDendritic CellsFlow CytometryCell biologyRatsmedicine.anatomical_structureGranzymePerforinCell cultureApoptosisbiology.proteinJournal of immunology (Baltimore, Md. : 1950)
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Quantitative analysis of opsonophagocytosis and of killing of Candida albicans by human peripheral blood leukocytes by using flow cytometry

1991

We describe a simple, rapid, automated procedure for measuring opsonophagocytosis and killing of Candida albicans by human peripheral blood leukocytes. Yeast cells are labelled by allowing uptake and cleavage of membrane-permeable bis-carboxyethyl-carboxyfluorescein pentaacetoxymethylester to its membrane-impermeable fluorescent derivative bis-carboxyethyl-carboxyfluorescein. The yeast cells are added to cell-rich plasma obtained after dextran sedimentation of erythrocytes. Opsonophagocytosis and killing are quantified by using automated fluorescent cell analysis, and the following parameters can be obtained: (i) relative percentage of phagocytes that participate in opsonophagocytosis, (ii)…

Cytotoxicity ImmunologicMicrobiology (medical)Phagocytemedicine.drug_classPhagocytosisIn Vitro TechniquesMonoclonal antibodyMicrobiologyFlow cytometryPhagocytosisCandida albicansLeukocytesmedicineHumansCandida albicansPhagocytesbiologymedicine.diagnostic_testOpsonin ProteinsFlow Cytometrybiology.organism_classificationMolecular biologyYeastCorpus albicansAntibody opsonizationmedicine.anatomical_structureEvaluation Studies as TopicResearch ArticleJournal of Clinical Microbiology
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Precursor frequency can compensate for lower TCR expression in T cell competition during priming in vivo.

2006

The factors controlling clonal dominance of cytotoxic T lymphocyte (CTL) responses are currently not well understood. To study the functional impact of the strength of the interaction of a T cell with an antigen-presenting cell in this context, we established a new mouse model comprised of two T cell receptor (TCR)-transgenic strains expressing the identical TCR in differing amounts, hence providing two CTL clones with different avidities but identical specificity and affinity. Utilizing this new model, we show that upon antigen challenge higher-avidity CTL expand at the expense of moderate-avidity CTL in vivo if present in equal numbers. Beyond this, moderate-avidity T cells can also contr…

Cytotoxicity ImmunologicT cellImmunologyReceptors Antigen T-CellPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicStreptamerImmunodominanceBiologyLymphocyte ActivationMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsAntigen PresentationStem CellsT-cell receptorhemic and immune systemsFlow CytometryAdoptive TransferCell biologyMice Inbred C57BLCTL*medicine.anatomical_structureImmunologyT-Lymphocytes CytotoxicEuropean journal of immunology
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Synthesis, chemical characterization, computational studies and biological activity of new DNA methyltransferases (DNMTs) specific inhibitor. Epigene…

2015

This work deals with the synthesis, the chemical characterization of dibutyltin(IV) complex of caffeic acid (Bu2Sn(IV)HCAF, caf1) and its cytotoxic action on tumor cells. The coordination environment at the tin center was investigated by FTIR, (119)Sn{(1)H} cross polarization magic angle spinning, electrospray ionization mass spectroscopy in the solid state and UV-vis, fluorescence and (1)H, (13)C and (119)Sn NMR spectroscopy in solution phases. Density functional theory study confirmed the proposed structures in solution phase and indicated the most probably stable conformation. The effects on viability of breast cancer MDA-MB231, colorectal cancer HCT116, hepatocellular carcinoma HepG2 an…

DNA (Cytosine-5-)-Methyltransferase 1Magnetic Resonance SpectroscopyMethyltransferaseAntineoplastic AgentsBiochemistryEpigenesis GeneticMembrane PotentialsInorganic Chemistrychemistry.chemical_compoundCaffeic AcidsCell Line TumorSettore BIO/10 - BiochimicaSpectroscopy Fourier Transform InfraredOrganotin CompoundsCaffeic acidHumansCytotoxic T cellDNA (Cytosine-5-)-MethyltransferasesEnzyme InhibitorsSettore CHIM/02 - Chimica FisicaChemistryOrganotin(IV) Caffeic acid DNMT1 DNA methylation CancerBiological activityDNA MethylationFlow CytometryMitochondriaModels ChemicalBiochemistryCell cultureSettore CHIM/03 - Chimica Generale E InorganicaDNA methylationHepatic stellate cellDNA
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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Processing of O6-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell …

2009

The DNA adduct O(6)-methylguanine (O(6)MeG) induced by environmental genotoxins and anticancer drugs is a highly mutagenic, genotoxic and apoptotic lesion. Apoptosis induced by O(6)MeG requires mismatch repair (MMR) and proliferation. Models of O(6)MeG-triggered cell death postulate that O(6)MeG/T mispairs activate MMR giving rise to either direct genotoxic signaling or secondary lesions that trigger apoptotic signaling in the 2(nd) replication cycle. To test these hypotheses, we used a highly synchronized cell system competent and deficient for the repair of O(6)MeG adducts, which were induced by the S(N)1 methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We show that DNA doub…

DNA ReplicationProgrammed cell deathMethylnitronitrosoguanidineCell cycle checkpointGuanineDNA repairBlotting WesternSuccinimidesApoptosisCHO CellsBiologychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductAnimalsDNA Breaks Double-StrandedMolecular BiologyCell CycleCell BiologyCell cycleFlow CytometryFluoresceinsMolecular biologyCell biologychemistryMicroscopy FluorescenceApoptosisDNA mismatch repairDNADevelopmental BiologyCell cycle (Georgetown, Tex.)
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Resveratrol, a chemopreventive agent, disrupts the cell cycle control of human SW480 colorectal tumor cells

2002

Resveratrol is a natural polyphenolic compound produced by a number of plants and found in high amount in peanuts, seeds, grapes or berries as source of human nutrition. Epidemiological studies strongly suggest that resveratrol may act as a cancer chemopreventive compound. The mechanism by which resveratrol inhibits cell proliferation was studied in human colorectal tumor SW480 cell line. The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner. Resveratrol appears to block the cell cycle at the transition --> G2/M since inhibition of [(3)H]-thymidine incorporation is not observed, while there is an increase of the c…

DNA Replicationendocrine system diseasesCellCyclin AAdenocarcinomaCyclin BProtein Serine-Threonine KinasesResveratrolS Phasechemistry.chemical_compoundCDC2 Protein KinaseStilbenesCDC2-CDC28 KinasesTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansCyclin B1Phosphorylationskin and connective tissue diseasesCyclinCyclin-dependent kinase 1biologyKinaseCell growthorganic chemicalsCell CycleCyclin-Dependent Kinase 2Cyclin-dependent kinase 2food and beveragesGeneral MedicineCell cycleFlow CytometryCyclin-Dependent KinasesGrowth InhibitorsNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureBiochemistrychemistryResveratrolEnzyme Inductionbiology.proteinCancer researchColorectal NeoplasmsProtein Processing Post-TranslationalCell DivisionInternational Journal of Molecular Medicine
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The Translesion Polymerase Rev3L in the Tolerance of Alkylating Anticancer Drugs

2009

Temozolomide and fotemustine, representing methylating and chloroethylating agents, respectively, are used in the treatment of glioma and malignant melanoma. Because chemoresistance of these tumors is a common phenomenon, identification of the underlying mechanisms is needed. Here we show that Rev3L, the catalytic subunit of the translesion DNA polymerase zeta, mediates resistance to both temozolomide and fotemustine. Rev3L knockout cells are hypersensitive to both agents. It is remarkable that cells heterozygous for Rev3L showed an intermediate sensitivity. Rev3L is not involved in the tolerance of the toxic O6-methylguanine lesion. However, a possible role of Rev3L in the tolerance of O6-…

DNA damageApoptosisDNA-Directed DNA PolymeraseBiologyNitrosourea CompoundsCell LineMiceOrganophosphorus CompoundsREV3LTemozolomidemedicineAnimalsAP siteAntineoplastic Agents AlkylatingPolymeraseMice KnockoutPharmacologyTemozolomideBase excision repairFlow CytometryMolecular biologyDNA-Binding ProteinsDacarbazineMicroscopy FluorescenceCancer researchbiology.proteinMolecular MedicineFotemustineDNA mismatch repairDrug Screening Assays AntitumorDNA Damagemedicine.drugMolecular Pharmacology
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Mutations in CTC1, encoding conserved telomere maintenance component 1, cause Coats plus

2012

Coats plus is a highly pleiotropic disorder particularly affecting the eye, brain, bone and gastrointestinal tract. Here, we show that Coats plus results from mutations in CTC1, encoding conserved telomere maintenance component 1, a member of the mammalian homolog of the yeast heterotrimeric CST telomeric capping complex. Consistent with the observation of shortened telomeres in an Arabidopsis CTC1 mutant and the phenotypic overlap of Coats plus with the telomeric maintenance disorders comprising dyskeratosis congenita, we observed shortened telomeres in three individuals with Coats plus and an increase in spontaneous γ 3H2AX-positive cells in cell lines derived from two affected individual…

DNA polymeraseMolecular Sequence DataTelomere-Binding ProteinsHistones/metabolismHDE GENHDE NEU PEDCST complexCEREBRORETINAL MICROANGIOPATHY FAMILIAL SYNDROME CALCIFICATIONS CYSTS PROTEIN DNA LEUKOENCEPHALOPATHY EVOLUTION DEFECTSHistoneschemistry.chemical_compoundAbnormalities Multiple/geneticsGeneticsmedicineAbnormalities MultipleGenetic Predisposition to DiseaseGeneticsTelomere-binding proteinTelomere/pathologyddc:618biologyBase SequenceGenetic Predisposition to Disease/geneticsDNA replicationSequence Analysis DNATelomeremedicine.diseaseFlow CytometryTelomereCell biologyRetinal Telangiectasis/genetics/pathologychemistrySequence Analysis DNA/methodsbiology.proteinRetinal TelangiectasisPrimaseTelomere-Binding Proteins/geneticsDNADyskeratosis congenitaNature Genetics
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In vivo fate mapping with SCL regulatory elements identifies progenitors for primitive and definitive hematopoiesis in mice.

2009

10 páginas, 6 figuras.-- et al.

Definitive hematopoiesisEmbryologyMyeloidPopulationConditional mouse modelIn vivo linage and fate tracingEmbryonic DevelopmentStem cell leukemia geneBiology03 medical and health sciencesMice0302 clinical medicineFate mappinghemic and lymphatic diseasesProto-Oncogene ProteinsCRE systemmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsCell LineageMesodermal blood cell specificationGene Knock-In TechniquesProgenitor celleducationGeneTetracycline systemT-Cell Acute Lymphocytic Leukemia Protein 1Primitive hematopoiesis030304 developmental biology0303 health scienceseducation.field_of_studyMicroscopy ConfocalStem CellsEmbryoFlow CytometryCell biologyHematopoiesisGastrulationHaematopoiesismedicine.anatomical_structureBlood cell precursors030220 oncology & carcinogenesisImmunologyIn vivo lineage markingDevelopmental BiologyMechanisms of development
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