Search results for "Myeloid"

showing 10 items of 538 documents

Detection of a TLR2 agonist by hematopoietic stem and progenitor cells impacts the function of the macrophages they produce

2013

Several groups have shown that detection of microbial components by TLRs on hematopoietic stem and progenitor cells (HSPCs) instructs myeloid cell generation, raising interest in the possibility of targeting TLRs on HSPCs to boost myelopoiesis. However, although "TLR-derived" cells exhibit myeloid cell characteristics (phagocytosis, cytokine production, antigen presentation), it is not clear whether they are functionally equivalent to macrophages derived in the absence of TLR activation. Our in vitro and in vivo studies show that macrophages derived from mouse and human HSPC subsets (including stem cells) exposed to a TLR2 agonist prior to or during macrophage differentiation produce lower …

Myeloidmedicine.medical_treatmentCellular differentiationImmunologyBiologyCell biologyHaematopoiesisCytokinemedicine.anatomical_structuremedicineImmunology and AllergyMacrophageMyelopoiesisStem cellProgenitor cellEuropean Journal of Immunology
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Participation of the cytokines interleukin 6, tumor necrosis factor-alpha, and interleukin 1-beta secreted by acute myelogenous leukemia blasts in au…

1989

Autonomous in vitro growth of myeloid leukemic colony-forming cells may in part result from autocrine production of colony-stimulating factors (CSF). Some acute myeloid leukemia (AML) samples, however, fail to synthesize CSF despite growing autonomously in agar, and are therefore believed to bypass CSF requirements. Cytokines such as IL-6, tumor necrosis factor (TNF)-alpha, and IL-1, products of cells of the myeloid lineage, are known to be involved in growth control of myeloid progenitor cells. Since these molecules may also contribute to autocrine and paracrine growth regulation of myeloid leukemias, we screened a series of AML for cytokine production. In addition, possible roles of IL-6,…

Myeloidmedicine.medical_treatmentMyeloid leukemiaGeneral MedicineBiologymedicine.diseaseColony-stimulating factorMyelogenousLeukemiaParacrine signallingmedicine.anatomical_structureCytokinehemic and lymphatic diseasesImmunologymedicineAutocrine signallingResearch Article
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Rôle de Tif1gamma dans les différenciations granulo-monocytaire et macrophagique

2015

Chronic myelomonocytic leukemia (CMML) is a hematologic stem cell disease whose characteristics correspond to myelodysplastic/myeloproliferative syndroms (MDS/MPS). Hematopoietic conditional deletion of Tif1γ in mice leads to the development of a MDS/MPS, mimiking human CMML, when age is comprised between 6 to 10 months, defining Tif1γ as a tumour suppressor gene. Moreover, peritoneal macrophage population in these mice is decreased despite a monocytosis.The aims of my work were first to characterize in sick mice the myeloid population, and second to study macrophage differentiation. The myeloid population in Tif1γΔ/Δ mice is morphologically immature, with granulocytic and monocytic feature…

Myelopoiesis[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyLeucémie myélomonocytaire chronique[SDV.BC]Life Sciences [q-bio]/Cellular BiologyChronic myelomonocytic leukemiaMyeloid-derived suppressor cellsTif1γ[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCellules myéloïdes suppressivesMyélopoïèse[SDV.BC] Life Sciences [q-bio]/Cellular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Cutting Edge: IL-1α Is a Crucial Danger Signal Triggering Acute Myocardial Inflammation during Myocardial Infarction

2016

Abstract Myocardial infarction (MI) induces a sterile inflammatory response that contributes to adverse cardiac remodeling. The initiating mechanisms of this response remain incompletely defined. We found that necrotic cardiomyocytes released a heat-labile proinflammatory signal activating MAPKs and NF-κB in cardiac fibroblasts, with secondary production of cytokines. This response was abolished in Myd88−/− fibroblasts but was unaffected in nlrp3-deficient fibroblasts. Despite MyD88 dependency, the response was TLR independent, as explored in TLR reporter cells, pointing to a contribution of the IL-1 pathway. Indeed, necrotic cardiomyocytes released IL-1α, but not IL-1β, and the immune acti…

MyocarditisImmunologyInterleukin-1betaMyocardial InfarctionInflammation030204 cardiovascular system & hematologyArticleProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineImmune system[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoInterleukin-1alphamedicineImmunology and AllergyAnimalsMyocytes CardiacMyocardial infarction030304 developmental biologyInflammationMice Knockout0303 health sciencesbusiness.industryToll-Like Receptorsmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMyocarditisIL1AImmunologyMyeloid Differentiation Factor 88Cancer researchmedicine.symptomSignal transductionbusinessSignal Transduction
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AIF-1 and RNASET2 are involved in the inflammatory response in the Mediterranean mussel Mytilus galloprovincialis following Vibrio infection

2022

Filter-feeding bivalves, such as the Mytilus species, are exposed to different types of bacteria in the surrounding waters, in particular of the Vibrio genus. Mussels lack an adaptive immune system and hemocytes can recognize pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs) to activate intracellular signaling pathways to trigger the antimicrobial effectors synthesis. Among the areas of bivalve immunity that deserve study include the role of hemocyte subpopulations. Since little information are available on immune responses at the tissue level to human pathogenic vibrios commonly detected in coastal waters involved in seafood-borne diseases, in this wor…

MytilusHemocytesTumor Suppressor ProteinsAIF-1 Bacterial challenge Cellular immunity Immunohistochemistrym M. galloprovincialis Myd88 RNASET2 TLR4RNASET2General MedicineAquatic ScienceAIF-1; Bacterial challenge; Cellular immunity; Immunohistochemistry; M. galloprovincialis; Myd88; RNASET2; TLR4Myd88ImmunohistochemistryCellular immunityToll-Like Receptor 4Bacterial challengeRibonucleasesSeafoodVibrio InfectionsMyeloid Differentiation Factor 88Environmental ChemistryAnimalsHumansTLR4M. galloprovincialisAIF-1Vibrio
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Synergistic targeting of FLT3 mutations in AML via combined menin-MLL and FLT3 inhibition

2020

Abstract The interaction of menin (MEN1) and MLL (MLL1, KMT2A) is a dependency and provides a potential opportunity for treatment of NPM1-mutant (NPM1mut) and MLL-rearranged (MLL-r) leukemias. Concomitant activating driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are particularly common in the NPM1mut subtype. In this study, transcriptional profiling after pharmacological inhibition of the menin-MLL complex revealed specific changes in gene expression, with downregulation of the MEIS1 transcription factor and its transcriptional target gene FLT3 being the most pronounced. Combining menin-MLL inhibition with specific small-molecule kinase inhibitors…

NPM1Transcription GeneticImmunologyApoptosisBiochemistryMiceRandom AllocationMice Inbred NODCell Line TumorProto-Oncogene Proteinshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsGene expressionmedicineAnimalsHumansMEN1PhosphorylationMyeloid Ecotropic Viral Integration Site 1 ProteinProtein Kinase InhibitorsneoplasmsbiologyGene Expression Regulation LeukemicKinaseNuclear ProteinsMyeloid leukemiaDrug SynergismHistone-Lysine N-MethyltransferaseCell BiologyHematologymedicine.diseaseCoculture TechniquesNeoplasm ProteinsLeukemia Myeloid AcuteLeukemiaKMT2Afms-Like Tyrosine Kinase 3biology.proteinCancer researchNucleophosminProtein Processing Post-TranslationalTyrosine kinaseMyeloid-Lymphoid Leukemia ProteinBlood
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The Mutational Landscape of Acute Myeloid Leukaemia Predicts Responses and Outcomes in Elderly Patients from the PETHEMA-FLUGAZA Phase 3 Clinical Tri…

2021

This article belongs to the Collection The Biomarkers for the Diagnosis and Prognosis in Cancer.

Neuroblastoma RAS viral oncogene homologOncologyCancer Researchgenetic riskMyeloid neoplasialeukemic cells0302 clinical medicinecytarabineclinical trials and observations:Other subheadings::/diagnosis [Other subheadings]MedicineComplete remissionazacytidineolder adultsRC254-282variantsLeukemiaAzacytidineHazard ratioleukemiaVariantsCytarabineacute:Neoplasms::Neoplasms by Histologic Type::Leukemia::Leukemia Myeloid::Leukemia Myeloid Acute [DISEASES]Neoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiaFludarabineLeukemiaOncology030220 oncology & carcinogenesisNGSOlder adultsLeucèmia mieloide aguda - Tractamentmyeloid neoplasiaMyelocyticmedicine.drugmedicine.medical_specialtymyelocyticcomplete remission:Otros calificadores::/diagnóstico [Otros calificadores]Subgroup analysisLeukemic cellsAcutePrognostic factorsArticle:neoplasias::neoplasias por tipo histológico::leucemia::leucemia mieloide::leucemia mieloide aguda [ENFERMEDADES]03 medical and health sciencesInternal medicineGenetic riskbusiness.industryprognostic factors:diagnóstico::pronóstico::resultado del tratamiento [TÉCNICAS Y EQUIPOS ANALÍTICOS DIAGNÓSTICOS Y TERAPÉUTICOS]Odds ratio:Diagnosis::Prognosis::Treatment Outcome [ANALYTICAL DIAGNOSTIC AND THERAPEUTIC TECHNIQUES AND EQUIPMENT]medicine.diseaseAvaluació de resultats (Assistència sanitària)CytarabinebusinessClinical trials and observations030215 immunology
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Molecular Characterization of Relapsed Core-Binding Factor (CBF) Acute Myeloid Leukemia (AML)

2015

Abstract Background: CBF-AML is defined by recurrent genetic abnormalities which encompass t(8;21)(q22;q22), inv(16)(p13.1q22) or less frequently t(16;16)(p13.1;q22). Most frequent secondary chromosome aberrations in t(8;21) AML are del(9q) or loss of a sex chromosome, and in inv(16)/t(16;16) AML trisomy 22 or trisomy 8. At the molecular level mutations involving KIT, FLT3, or NRAS were identified as recurrent lesions in CBF-AML. However, the underlying genetic alterations which might trigger relapse in CBF-AML are not well delineated. Thus, the aim of our study was to characterize the clonal architecture of relapsed CBF-AML. Methods: We performed mutational profiling (KIT, FLT3-ITD, FLT3-T…

Neuroblastoma RAS viral oncogene homologOncologymedicine.medical_specialtybusiness.industryImmunologyMyeloid leukemiaCell BiologyHematologyKit mutationCore binding factorBioinformaticsTrisomy 8medicine.diseaseBiochemistryExonInternal medicineChromosome abnormalityMedicinebusinessTrisomyBlood
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Steady-state neutrophil homeostasis is dependent on TLR4/TRIF signaling

2013

Polymorphonuclear neutrophil granulocytes (neutrophils) are tightly controlled by an incompletely understood homeostatic feedback loop adjusting the marrow's supply to peripheral needs. Although it has long been known that marrow cellularity is inversely correlated with G-CSF levels, the mechanism linking peripheral clearance to production remains unknown. Herein, the feedback response to antibody induced neutropenia is characterized to consist of G-CSF–dependent shifts of marrow hematopoietic progenitor populations including expansion of the lin-/Sca-1/c-kit (LSK) and granulocyte macrophage progenitor (GMP) compartments at the expense of thrombopoietic and red cell precursors. Evidence is …

NeutrophilsImmunologyRecombinant Granulocyte Colony-Stimulating FactorBiologyBiochemistryGranulopoiesisMiceGranulocyte Colony-Stimulating FactorAnimalsHomeostasisGranulocyte Precursor CellsLymphocytesNeutrophil homeostasisReceptorMice KnockoutCell BiologyHematologyGranulocyte colony-stimulating factorToll-Like Receptor 4Adaptor Proteins Vesicular TransportTRIFMyeloid Differentiation Factor 88ImmunologyTLR4HomeostasisSignal TransductionBlood
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Midostaurin Plus Intensive Chemotherapy for Younger and Older Patients with Acute Myeloid Leukemia and FLT3 Internal Tandem Duplications

2021

Abstract BACKGROUND: Midostaurin is a first-generation, type I multi-targeted kinase inhibitor with inhibitory activity against FLT3-ITD and -TKD mutations. Midostaurin is approved by FDA and EMA in combination with intensive induction and consolidation chemotherapy for adult patients with AML exhibiting an activating FLT3 mutation; the EMA label also includes single-agent maintenance therapy following consolidation chemotherapy. We conducted a phase-II trial (AMLSG 16-10) to evaluate midostaurin with induction chemotherapy followed by allogeneic hematopoietic-cell transplantation (HCT) and a one-year midostaurin maintenance therapy in younger and older patients with acute myeloid leukemia …

Oncology0303 health sciencesmedicine.medical_specialtybusiness.industryImmunologyMyeloid leukemiaCell BiologyHematologyIntensive chemotherapyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOlder patientschemistryInternal medicinemedicineMidostaurinbusiness030304 developmental biology030215 immunologyBlood
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