Search results for "Colony-Stimulating Factor"

showing 10 items of 174 documents

A newly established murine immature dendritic cell line can be differentiated into a mature state, but exerts tolerogenic function upon maturation in…

2007

AbstractThe phenotype and function of murine dendritic cells (DCs) are primarily studied using bone-marrow–derived DCs (BM-DCs), but may be hampered by the heterogenous phenotype of BM-DCs due to their differential state of maturation. Here we characterize a newly established murine DC line (SP37A3) of myeloid origin. During maintainance in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and M-CSF, SP37A3 cells resemble immature DCs characterized by low expression of major histocompatibility complex (MHC) II and costimulatory molecules and low T-cell stimulatory capacity. Upon stimulation, SP37A3 cells acquire a mature phenotype and activate naive T cells as potent…

Macrophage colony-stimulating factorMyeloidmedicine.medical_treatmentImmunologyBiologyMajor histocompatibility complexT-Lymphocytes RegulatoryBiochemistryDexamethasoneCell LineMicemedicineAnimalsGlucocorticoidsMyeloid Progenitor CellsCell ProliferationClonal AnergyMice Inbred BALB CFollicular dendritic cellsReceptors IgGHistocompatibility Antigens Class IICell DifferentiationDendritic CellsCell BiologyHematologyDendritic cellCoculture TechniquesUp-RegulationCell biologyInterleukin 1 Receptor Antagonist ProteinGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureCytokineCell culturebiology.proteinCytokinesmedicine.drugBlood
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Granulocyte-macrophage colony-stimulating factor induces cytokine secretion by human polymorphonuclear leukocytes.

1989

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous…

Macrophage colony-stimulating factorNeutrophilsT cellInflammationBiologyBiological FactorsMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineAnimalsHumansRNA MessengerGrowth SubstancesTumor Necrosis Factor-alphaMacrophage Colony-Stimulating FactorLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGeneral MedicineColony-stimulating factorRecombinant ProteinsRetractionCell biologymedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyCytokinesTumor necrosis factor alphaCytokine secretionmedicine.symptomResearch Articlemedicine.drugJournal of Clinical Investigation
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CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

2009

金沢大学医薬保健研究域医学系

Macrophage colony-stimulating factorPathologymedicine.medical_specialtymedicine.medical_treatmenteducation030232 urology & nephrologyApoptosisReceptor Macrophage Colony-Stimulating FactorBiology03 medical and health sciencesParacrine signallingMice0302 clinical medicineFibrosismedicineAnimalsHumansRegenerationAutocrine signalling030304 developmental biologyCell Proliferation0303 health sciencesMice Inbred C3HGrowth factorMacrophage Colony-Stimulating FactorMacrophageshemic and immune systemsEpithelial CellsGeneral Medicinemedicine.diseaseFibrosis3. Good healthKidney TubulesIntegrin alpha MApoptosisReperfusion Injurybiology.proteinCancer researchReperfusion injurytissuesResearch Article
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Production of macrophage-, granulocyte-, granulocyte-macrophage- and multi-colony-stimulating factor by peripheral blood cells

1989

The specific cell sources and signals for induction of various colony-stimulating factors (CSF) in peripheral blood mononuclear cells (PBMC), purified T lymphocyte and monocyte (Mo) populations have been investigated. In the absence of exogenous activating stimuli, human PBMC, T cells and Mo failed to produce stable cytoplasmic mRNA for CSF for macrophages (M-CSF or CSF-1), for granulocytes (G-CSF), for granulocytes and macrophages (GM-CSF) and for multilineage CSF [multi-CSF, interleukin (IL) 3] and thus failed to release CSF proteins. However, after stimulation with phorbol myristate acetate and phytohemagglutinin, M-, G-, GM- and multi-CSF mRNA became detectable in PBMC, resulting in the…

Macrophage colony-stimulating factorT-Lymphocytesmedicine.medical_treatmentImmunologyGranulocyteBiologyPeripheral blood mononuclear cellMonocytesColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineHumansImmunology and AllergyMacrophageRNA MessengerGrowth SubstancesMacrophage Colony-Stimulating FactorMonocyteGranulocyte-Macrophage Colony-Stimulating FactorT lymphocyteMolecular biologyGranulocyte macrophage colony-stimulating factorCytokinemedicine.anatomical_structureImmunologyInterleukin-3medicine.drugEuropean Journal of Immunology
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Alpha-defensins secreted by dysplastic granulocytes inhibit the differentiation of monocytes in chronic myelomonocytic leukemia.

2010

Abstract Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic disorder that occurs in elderly patients. One of the main diagnostic criteria is the accumulation of heterogeneous monocytes in the peripheral blood. We further explored this cellular heterogeneity and observed that part of the leukemic clone in the peripheral blood was made of immature dysplastic granulocytes with a CD14−/CD24+ phenotype. The proteome profile of these cells is dramatically distinct from that of CD14+/CD24− monocytes from CMML patients or healthy donors. More specifically, CD14−/CD24+ CMML cells synthesize and secrete large amounts of alpha-defensin 1-3 (HNP1-3). Recombinant HNPs inhibit macrophage co…

Macrophage colony-stimulating factoralpha-DefensinsCD14Cellular differentiationImmunologyLipopolysaccharide ReceptorsChronic myelomonocytic leukemiaUridine TriphosphateBiologyGranulocyteBiochemistryMonocytesUridine DiphosphatemedicineMacrophageHumansReceptors Purinergic P2MonocyteMacrophage Colony-Stimulating FactorMacrophagesCD24 AntigenCell DifferentiationLeukemia Myelomonocytic ChronicCell BiologyHematologymedicine.diseaseHaematopoiesismedicine.anatomical_structureCancer researchCytokinesGranulocytesBlood
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Tumor necrosis factor (TNF)-alpha but not TNF-beta induces secretion of colony stimulating factor for macrophages (CSF-1) by human monocytes

1987

Abstract Tumor necrosis factor (TNF)-alpha has been identified as a major inducer of colony stimulating factor (CSF)-secretion by human vascular endothelial cells and fibroblasts. In the present study we assessed the capacity of TNFs to induce release of CSF-1 from highly purified peripheral blood monocyte preparations. Whereas monocytes do not accumulate CSF-1 messenger (m)RNA constitutively and consequently do not produce CSF-1 protein, CSF-1 mRNA and protein secretion became detectable, when monocytes were cultured in the presence of TNF-alpha, that was synergistically enhanced by interferon-gamma (IFN-gamma). However, under identical experimental conditions TNF-beta failed to induce mon…

Macrophage colony-stimulating factormedicine.medical_specialtyT-LymphocytesImmunologyIn Vitro TechniquesBiologyBiochemistryMonocytesColony-Forming Units AssayColony-Stimulating FactorsInternal medicinemedicineHumansSecretionLeukapheresisMessenger RNATumor Necrosis Factor-alphaMonocyteCell BiologyHematologyMacrophage ActivationColony-stimulating factorMolecular biologyHaematopoiesisEndocrinologySecretory proteinmedicine.anatomical_structureTumor necrosis factor alphaBlood
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The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema

2018

Hereditary angioedema (HAE) is a rare autosomic-dominant disorder characterized by a deficiency of C1 esterase inhibitor which causes episodic swellings of subcutaneous tissues, bowel walls and upper airways that are disabling and potentially life-threatening. We evaluated n = 17 patients with confirmed HAE diagnosis during attack and remission state and n = 19 healthy subjects. The samples were tested for a panel of IL (Interleukin)-17-type cytokines (IL-1β, IL-6, IL-10, granulocyte–macrophage colony stimulating factor (GM-CSF), IL-17, IL-21, IL-22, IL-23) and transforming growth factor-beta (TGF-β) subtypes. Data indicate that there are variations of cytokine levels in HAE subjects compar…

Male0301 basic medicinemedicine.medical_treatmentC1 esterase inhibitorInterleukin-23chemistry.chemical_compoundSubcutaneous TissueTransforming Growth Factor betaChildHereditary angioedemaHematologyInterleukin-17InterleukinGeneral MedicineMiddle AgedIntestinesCytokineHereditary angioedemaFemaleInterleukin 17medicine.symptomComplement C1 Inhibitor ProteinAdultmedicine.medical_specialtyAdolescentBradykininBronchiBradykininGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInternal medicinemedicineHumansCytokineAgedBiochemistry Genetics and Molecular Biology (all)Angioedemabusiness.industryInterleukinsAngioedemas HereditaryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseColony-stimulating factor030104 developmental biologyGene Expression RegulationchemistryCase-Control StudiesImmunologyTh17 CellsbusinessClinical and Experimental Medicine
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Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.

2011

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic ce…

MaleAgingAntimetabolites AntineoplasticTumor suppressor geneCellular differentiationMolecular Sequence DataChronic myelomonocytic leukemiaReceptor Macrophage Colony-Stimulating FactorBiologyDecitabinechemistry.chemical_compoundMicemedicineAnimalsHumansGenes Tumor SuppressorPromoter Regions GeneticTranscription factorAgedAged 80 and overMice KnockoutBase SequenceGene Expression Regulation LeukemicCell DifferentiationLeukemia Myelomonocytic ChronicGeneral MedicineDNA MethylationMiddle Agedmedicine.diseaseTRIM33Hematopoietic Stem CellsMolecular biologyDemethylating agentHematopoiesisNeoplasm ProteinsSpecific Pathogen-Free OrganismsHaematopoiesischemistryDNA methylationCancer researchAzacitidineFemaleTranscription FactorsResearch ArticleThe Journal of clinical investigation
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Incidence and risk factors of post-engraftment invasive fungal disease in adult allogeneic hematopoietic stem cell transplant recipients receiving or…

2015

Studies that analyze the epidemiology and risk factors for invasive fungal disease (IFD) after engraftment in alloSCT are few in number. This single-center retrospective study included 404 alloSCT adult recipients surviving > 40 days who engrafted and were discharged without prior IFD. All patients who received >= 20 mg/day of prednisone were assigned to primary oral prophylaxis (itraconazole or low-dose voriconazole). The primary end point was the cumulative incidence (CI) of probable/proven IFD using the European Organization for Research and Treatment of Cancer and Mycoses Study Group (EORTC/MSG) criteria. The independent prognostic factors after multivariate analyses were used to constr…

MaleAntifungal AgentsTransplantation ConditioningPremedicationmedicine.medical_treatmentMULTICENTERAdministration OralHematopoietic stem cell transplantationEchinocandinsCOMPETING RISKCaspofunginRisk FactorsCause of DeathINFECTIONGranulocyte Colony-Stimulating FactorEPIDEMIOLOGYCumulative incidenceTreatment FailureFramingham Risk ScoreIncidenceIncidence (epidemiology)Hematopoietic Stem Cell TransplantationHematologyMiddle AgedAllograftsHematologic NeoplasmsVORICONAZOLEDrug Therapy CombinationFemaleASPERGILLOSISRisk assessmentFungemiamedicine.drugAdultmedicine.medical_specialtyNeutropeniaANTIFUNGAL PROPHYLAXISNeutropeniaRisk AssessmentITRACONAZOLEMedication AdherenceImmunocompromised HostLipopeptidesYoung AdultAmphotericin BInternal medicinemedicineAspergillosisHumansAgedRetrospective StudiesVoriconazoleTransplantationbusiness.industryRetrospective cohort studyFLUCONAZOLETriazolesmedicine.diseaseSurvival AnalysisSurgeryMycosesPatient CompliancebusinessSCT
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Granulocyte-macrophage-colony-stimulating factor enhances immune responses to melanoma-associated peptides in vivo.

1996

Peptide epitopes derived from differentiation antigens of the melanocyte lineage were recently identified in human melanomas as targets for MHC-restricted cytotoxic T lymphocytes (CTL). The characterization of multiple CTL-defined antigenic determinants has opened possibilities of development of antigen-targeted vaccines. In the present study, we determined CTL reactivity against melanoma-associated peptides derived from Melan A/MART-1, tyrosinase, and gp100/Pmel17 in 3 HLA-A2+ melanoma patients. Then, we assessed the immune responses to synthetic melanoma-associated peptides injected intradermally. After 3 cycles of immunization with peptide alone, we used systemic GM-CSF as an adjuvant du…

MaleCancer ResearchCellular immunitymedicine.medical_treatmentMolecular Sequence Data10050 Institute of Pharmacology and Toxicology610 Medicine & healthchemical and pharmacologic phenomenaActive immunizationEpitopeImmune systemAntigenAdjuvants ImmunologicAntigens NeoplasmmedicineCytotoxic T cellHumans1306 Cancer ResearchHypersensitivity DelayedAmino Acid SequenceMelanomabusiness.industryGranulocyte-Macrophage Colony-Stimulating FactorImmunotherapyMiddle AgedImmunohistochemistryNeoplasm ProteinsCTL*OncologyImmunology570 Life sciences; biology2730 OncologyFemaleImmunizationbusinessMelanoma-Specific AntigensT-Lymphocytes CytotoxicInternational journal of cancer
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