Search results for "proliferation"

showing 10 items of 1193 documents

Regulatory T cells selectively preserve immune privilege of self-antigens during viral central nervous system infection.

2012

Abstract Regulatory T cells (Tregs) are important for the attenuation of immune reactions. During viral CNS infections, however, an indiscriminate maintenance of CNS immune privilege through Treg-mediated negative regulation could prevent autoimmune sequelae but impair the control of viral replication. We analyzed in this study the impact of Tregs on the development of acute viral encephalomyelitis, T cell-mediated antiviral protection, and prevention of CNS autoimmunity following intranasal infection with the gliatropic mouse hepatitis virus strain A59. To assess the contribution of Tregs in vivo, we specifically depleted CD4+Foxp3+ T cells in a diphtheria toxin-dependent manner. We found …

Receptors CXCR3T cellImmunologychemical and pharmacologic phenomenaAutoimmunityBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeCXCR3Lymphocyte ActivationAutoantigensT-Lymphocytes RegulatoryLymphocyte DepletionAutoimmunity03 medical and health sciencesMice0302 clinical medicineCentral Nervous System InfectionsImmune privilegeImmunitymedicineImmunology and AllergyAnimalsHumansEncephalomyelitisAdministration Intranasal030304 developmental biologyCell Proliferation0303 health sciencesImmunity CellularMice Inbred BALB CMurine hepatitis virusFOXP3hemic and immune systemsForkhead Transcription Factors3. Good healthmedicine.anatomical_structureViral replicationImmunologyAcute DiseaseCD4 AntigensLymph NodesCoronavirus InfectionsCD8030215 immunologyJournal of immunology (Baltimore, Md. : 1950)
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Requirement of Retinoic Acid Receptor Isotypes α, β, and γ during the Initial Steps of Neural Differentiation of PCC7 Cells

2005

Retinoic acid (RA) is indispensable for morphogenesis and differentiation of several tissues, including the nervous system. The requirement of the RA receptor (RAR) isotypes alpha, beta, and gamma and the putative role of retinoid X receptor-(RXR) signaling in RA-induced neural differentiation, was analyzed. For this compound-selective retinoids and the murine embryonal carcinoma cell line PCC7, a model system for RA-dependent neural differentiation was used. The present paper shows that proliferating PCC7 cells primarily express RXRalpha and RARalpha, lower levels of RXRbeta, and barely detectable amounts of RARbeta, RARgamma, and RXRgamma. At receptor-selective concentrations, only a RARa…

Receptors Retinoic AcidRetinoic acidReceptors Cytoplasmic and NuclearApoptosisLigandsMicechemistry.chemical_compoundEndocrinologyGenes ReporterNuclear Receptor Subfamily 6 Group A Member 1Protein IsoformsRetinoidReceptorGlutathione TransferaseNeuronsCell DeathReverse Transcriptase Polymerase Chain ReactionCell DifferentiationGeneral MedicineImmunohistochemistryUp-RegulationCell biologyDNA-Binding ProteinsBiochemistrySignal transductionPlasmidsProtein BindingSignal Transductionmedicine.drugTranscriptional ActivationDNA Complementarymedicine.drug_classRecombinant Fusion ProteinsBlotting WesternDown-RegulationTretinoinRetinoid X receptorBiologyTransfectionCell LineTretinoinCell Line TumormedicineAnimalsHumansMolecular BiologyCell ProliferationKineticsRetinoic acid receptorRetinoid X ReceptorschemistryNuclear receptorRNAOctamer Transcription Factor-3Transcription FactorsMolecular Endocrinology
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Macrophage migration inhibitory factor is critically involved in basal and fluoxetine-stimulated adult hippocampal cell proliferation and in anxiety,…

2011

Intensive research is devoted to unravel the neurobiological mechanisms mediating adult hippocampal neurogenesis, its regulation by antidepressants, and its behavioral consequences. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that is expressed in the CNS, where its function is unknown. Here, we show, for the first time, the relevance of MIF expression for adult hippocampal neurogenesis. We identify MIF expression in neurogenic cells (in stem cells, cells undergoing proliferation, and in newly proliferated cells undergoing maturation) in the subgranular zone of the rodent dentate gyrus. A causal function for MIF in cell proliferation was shown using genetic (M…

Receptors SteroidStem-Cellsanimal diseasesmedicine.medical_treatmentHippocampusExpressionHippocampal formationHippocampusSubgranular zonememoryMice0302 clinical medicineConditioning PsychologicalCyclin D2Rat Dentate GyrusMice KnockoutNeurons0303 health sciencesMicroscopy ConfocalChronic StressMifNeurogenesisBrainFearrespiratory systemanxietyPsychiatry and Mental healthC-Reactive ProteinCytokinemedicine.anatomical_structuredepressionAntidepressive Agents Second-GenerationStem cellPsychologyAnimal-ModelNeurogenesisSpatial BehaviorNerve Tissue Proteinschemical and pharmacologic phenomena03 medical and health sciencesCellular and Molecular Neurosciencemedicineotorhinolaryngologic diseasesAnimalsRats WistarMaze LearningMacrophage Migration-Inhibitory FactorsMolecular BiologyCell Proliferation030304 developmental biologyMemory DisordersDentate gyrusfluoxetineFactor Mifbiological factorsRatsDisease Models AnimalAcoustic StimulationBromodeoxyuridineMacrophage migration inhibitory factorCorticosteroneNeuroscience030217 neurology & neurosurgery
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Intercellular communication and human hepatocellular carcinoma.

2005

We have previously reported that gap junction-mediated intercellular communication (GJIC) can be restored in junctionally deficient human prostate epithelial cells, also suggesting that GJIC activity is regulated by estrogen. In the present work, we report studies on sex steroid regulation of GJIC and proliferative activity in both nontumoral (Chang liver, CL) and malignant (HepG2, Huh7) human liver cells. Junctional activity and liver cell growth were measured using the scrape-loading/dye-transfer (SL/DT) and the MTS assay, respectively. Using the SL/DT, only Huh7 cells exhibited a moderate degree of Junctional activity in basic conditions, while neither CL nor HepG2 cells showed functiona…

Receptors SteroidTime FactorsProliferationCell Communicationchemistry.chemical_compoundNeoplasmsReceptorTumorGeneral NeuroscienceLiver cellLiver NeoplasmsGap JunctionsGap junction-mediated intercellular communication (GJIC)ImmunohistochemistryLiverLiver NeoplasmReceptors AndrogenGap JunctionReceptors ProgesteroneHumanmedicine.medical_specialtyCell signalingCarcinoma HepatocellularTime Factormedicine.drug_classEstroneBiologyGeneral Biochemistry Genetics and Molecular BiologyCell LineHistory and Philosophy of ScienceInternal medicineCell Line TumormedicineCarcinomaEstrogen Receptor betaHumansHepatocellular carcinoma (HCC)SteroidCell ProliferationBiochemistry Genetics and Molecular Biology (all)Cell growthEstrogen Receptor alphamedicine.diseasedigestive system diseasesEndocrinologychemistryEstrogenCell cultureCancer researchNeoplasmAnnals of the New York Academy of Sciences
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Gene Regulation of Peroxisomal Enzymes by Nutrients, Hormones and Nuclear Signalling Factors in Animal and Human Species

2003

Many peroxisomal enzymes are controlled at the transcriptional level. This gene regulation is well documented in liver from rodent species and is more important upon peroxisome proliferation, although both phenomena are not always associated. Understanding of this regulation comes largely from studies on PPARs (Peroxisome Proliferator-Activated Receptors). Other transcription factors including thyroid hormone receptors, glucocorticoid receptors, LXR, also influence peroxisomal gene expression often in combination with tissue specific cofactors (co-activators or co-repressors). In human tissues and cells, inducibility of peroxisomal enzymes often has not been investigated. De Craemer (1995) …

Regulation of gene expressionPristanic acidchemistry.chemical_compoundchemistryBiochemistryPeroxisome ProliferationPeroxisomeBiologyReceptorLiver X receptorTranscription factorPPAR agonist
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Tumor cells convert immature myeloid dendritic cells into TGF-β–secreting cells inducing CD4+CD25+ regulatory T cell proliferation

2005

The mechanisms through which regulatory T cells accumulate in lymphoid organs of tumor-bearing hosts remain elusive. Our experiments indicate that the accumulation of CD4+CD25+ regulatory T cells (T reg cells) expressing FoxP3 and exhibiting immunosuppressive function originates from the proliferation of naturally occurring CD25+ T cells and requires signaling through transforming growth factor (TGF)–β receptor II. During tumor progression, a subset of dendritic cells (DCs) exhibiting a myeloid immature phenotype is recruited to draining lymph nodes. This DC subset selectively promotes the proliferation of T reg cells in a TGF-β–dependent manner in mice and rats. Tumor cells are necessary a…

Regulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryArticleMiceInterleukin 21Transforming Growth Factor betaCell Line TumorNeoplasmsmedicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCell ProliferationDNA PrimersInterleukin 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationForkhead Transcription FactorsRats Inbred Strainshemic and immune systemsDendritic CellsNatural killer T cellImmunohistochemistryMolecular biologyRatsCell biologymedicine.anatomical_structureBromodeoxyuridineInterleukin 12Receptors Transforming Growth Factor betaSignal TransductionJournal of Experimental Medicine
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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Proliferative activity in stenotic human aortocoronary bypass grafts

2002

Abstract Background: Aortocoronary bypass graft disease is responsible for long-term failure of autologous vein grafts. The analyses of proliferation and cell type characterisation in human bypass grafts harvested during re-do surgery make it possible to investigate the cellular processes leading to bypass graft failure. Methods: 30 stenotic vein grafts and 25 control veins were explantated during re-do heart surgery procedures. The total area and cell count of the neointima, media and adventitia were calculated computer-assisted. Actively proliferating cells were identified using antibody to Ki-67 and positive cells were determined by double-label immunocytochemistry with SMC α-actin, CD 3…

ReoperationNeointimaCell typemedicine.medical_specialtyPathologyProliferation indexT-LymphocytesImmunocytochemistryCellCell CountBypass graftsMuscle Smooth VascularPathology and Forensic MedicineAntigens CDAdventitiaInternal medicineHumansMedicineSaphenous VeinCoronary Artery Bypassbiologybusiness.industryMacrophagesGraft SurvivalGraft Occlusion VascularGeneral MedicineImmunohistochemistryActinsKi-67 Antigenmedicine.anatomical_structurecardiovascular systembiology.proteinCardiologyAntibodyCardiology and Cardiovascular MedicinebusinessBiomarkersCell DivisionCardiovascular Pathology
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Ki-67 assessment of pancreatic neuroendocrine neoplasms: Systematic review and meta-analysis of manual vs. digital pathology scoring

2022

Ki-67 assessment is a key step in the diagnosis of neuroendocrine neoplasms (NENs) from all anatomic locations. Several challenges exist related to quantifying the Ki-67 proliferation index due to lack of method standardization and inter-reader variability. The application of digital pathology coupled with machine learning has been shown to be highly accurate and reproducible for the evaluation of Ki-67 in NENs. We systematically reviewed all published studies on the subject of Ki-67 assessment in pancreatic NENs (PanNENs) employing digital image analysis (DIA). The most common advantages of DIA were improvement in the standardization and reliability of Ki-67 evaluation, as well as its spee…

Reproducibility of ResultsBreast NeoplasmsCarcinoid TumorPathology and Forensic MedicinePancreatic Neoplasmsneuroendocrine neoplasms pancreasNeuroendocrine TumorsKi-67 AntigenGastroenteropancreatic Neuroendocrine TumorBiomarkers TumorImage Processing Computer-AssistedHumansGastroenteropancreatic Neuroendocrine Tumor; Cancer; Carcinoid TumorFemaleCell ProliferationCancer
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The topology of vitronectin: A complementary feature for neuroblastoma risk classification based on computer‐aided detection

2019

Tumors are complex networks of constantly interacting elements: tumor cells, stromal cells, immune and stem cells, blood/lympathic vessels, nerve fibers and extracellular matrix components. These elements can influence their microenvironment through mechanical and physical signals to promote tumor cell growth. To get a better understanding of tumor biology, cooperation between multidisciplinary fields is needed. Diverse mathematic computations and algorithms have been designed to find prognostic targets and enhance diagnostic assessment. In this work, we use computational digital tools to study the topology of vitronectin, a glycoprotein of the extracellular matrix. Vitronectin is linked to…

RiskCancer ResearchStromal celltopologyTumor Markers and SignaturesComputer scienceAngiogenesisTopologyTopologyvitronectinExtracellular matrixComputational biology03 medical and health sciencesNeuroblastoma0302 clinical medicinecomputational biologyNeuroblastNeuroblastomamedicineTumor MicroenvironmentHumansVitronectinCell ProliferationbiologyNeovascularization PathologicComplex networkmedicine.diseasePrognosisExtracellular MatrixOncology030220 oncology & carcinogenesisnetworksbiology.proteinVitronectinStem cellNetworksStromal CellsAlgorithmsInternational Journal of Cancer
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