Search results for "Myeloid"

showing 10 items of 538 documents

Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4

2012

Ingestion of wheat, barley, or rye triggers small intestinal inflammation in patients with celiac disease. Specifically, the storage proteins of these cereals (gluten) elicit an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. This well-defined role of adaptive immunity contrasts with an ill-defined component of innate immunity in celiac disease. We identify the α-amylase/trypsin inhibitors (ATIs) CM3 and 0.19, pest resistance molecules in wheat, as strong activators of innate immune responses in monocytes, macrophages, and dendritic cells. ATIs engage the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers a…

GliadinMice0302 clinical medicineHEK293 CellImmunology and AllergyTriticumPlant Proteins2. Zero hungerMice Knockout0303 health sciencesToll-like receptorMice Inbred C3Hfood and beveragesPlant ProteinU937 CellsAcquired immune system3. Good health030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsHumanSignal TransductionImmunologyMolecular Sequence DataInflammationBiologyProinflammatory cytokineCell Line03 medical and health sciencesImmune systemImmunitymedicineAnimalsHumansAmino Acid Sequence030304 developmental biologyInnate immune systemSequence Homology Amino AcidAnimalBIO/13 - BIOLOGIA APPLICATAnutritional and metabolic diseasesHordeumImmunity InnateToll-Like Receptor 4Mice Inbred C57BLCeliac DiseaseHEK293 CellsImmunologyMyeloid Differentiation Factor 88TLR4Trypsin Inhibitor
researchProduct

Role of colony‐stimulating factors in the biology of acute myelogenous leukemia

1989

A high proportion of acute myeloid leukemias (AML) recently investigated for their capacity to synthesize biologically active bioregulatory molecules was found to accumulate messenger (m) RNA and to produce membrane-bound or -secreted forms of stimulating factors for granulocyte, macrophage and mixed granulocyte-macrophage colony growth. Blast cells have also been found to secrete interleukin 1, tumor necrosis factor-alpha, interleukin 6, and to express receptors for various growth factors as well. However, growth factors like interleukin 2 and interleukin 3 have not been identified as AML products, and several other factors including interleukin 4, interleukin 5, etc. need further evaluati…

Growth factormedicine.medical_treatmentInterleukinCell BiologyBiologyLeukemia Myeloid AcuteInterleukin 20Colony-Stimulating FactorsImmunologyCancer researchmedicineInterleukin 12biology.proteinHumansInterleukin 6Interleukin 5Interleukin 4Interleukin 3The International Journal of Cell Cloning
researchProduct

Direct Toll-Like Receptor-Mediated Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Macropha…

2012

Abstract As Toll-like receptors (TLRs) are expressed by hematopoietic stem and progenitor cells (HSPCs), they may play a role in hematopoiesis in response to pathogens during infection. We show here that TLR2, TLR4, and TLR9 agonists (tripalmitoyl-S-glyceryl-L-Cys-Ser-(Lys)4 [Pam3CSK4], lipopolysaccharide [LPS], and CpG oligodeoxynucleotide [ODN]) induce the in vitro differentiation of purified murine lineage negative cells (Lin−) as well as HSPCs (identified as Lin− c-Kit+ Sca-1+ IL-7Rα− [LKS] cells) toward macrophages (Mph), through a myeloid differentiation factor 88 (MyD88)-dependent pathway. In order to investigate the possible direct interaction of soluble microorganism-associated mol…

Hematopoietic stem and progenitor cellsBiologyCell LineMicemedicineAnimalsProgenitor cellToll-like receptorInnate immune systemMacrophagesToll-Like ReceptorsTLR9Cell DifferentiationCell BiologyFlow CytometryHematopoietic Stem CellsMyD88Molecular biologyToll-Like Receptor 2Toll-like receptorsMice Inbred C57BLToll-Like Receptor 4TLR2Haematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88TLR4Molecular MedicineBone marrowDevelopmental BiologySignal Transduction
researchProduct

Macrophage MerTK promotes profibrogenic cross-talk with hepatic stellate cells via soluble mediators

2022

Background & aims: Activation of Kupffer cells and recruitment of monocytes are key events in fibrogenesis. These cells release soluble mediators which induce the activation of hepatic stellate cells (HSCs), the main fibrogenic cell type within the liver. Mer tyrosine kinase (MerTK) signaling regulates multiple processes in macrophages and has been implicated in the pathogenesis of non-alcoholic steatohepatitis-related fibrosis. In this study, we explored if MerTK activation in macrophages influences the profibrogenic phenotype of HSCs. Methods: Macrophages were derived from THP-1 cells or differentiated from peripheral blood monocytes towards MerTK+/CD206+/CD163+/CD209- macrophages. Th…

HepatologyCM conditioned medium ECM extracellular matrix Gas-6 Gas-6 growth arrest-specific gene 6 HSC(s) hepatic stellate cells KC(s) Kupffer cell(s) M-CSF macrophage colony-stimulating factor M2c-like macrophages MerTK Myeloid-epithelial-reproductive tyrosine kinase NAFLD non-alcoholic fatty liver disease NASH NASH non-alcoholic steatohepatitis PMA phorbol 12-myristate 13-acetate TGFβ1 transforming growth factor-β1 THP-1 TIMP1 tissue inhibitor of metalloproteinase 1 VEGF-A vascular endothelial growth factor-A liver fibrosis siRNA small-interfering RNAGas-6; liver fibrosis; M2c-like macrophages; NASH; THP-1GastroenterologyInternal MedicineImmunology and AllergyJHEP Reports
researchProduct

The role of the human cytomegalovirus UL111A gene in down-regulating CD4+ T-cell recognition of latently infected cells: implications for virus elimi…

2009

AbstractThe capacity of human cytomegalovirus (HCMV) to establish and maintain a latent infection from which it can later reactivate ensures its widespread distribution in the population, but the mechanisms enabling maintenance of latency in the face of a robust immune system are poorly understood. We examined the role of the HCMV UL111A gene, which encodes homologs of the immunosuppressive cytokine interleukin-10 in the context of latent infection of myeloid progenitor cells. A UL111A deletion virus was able to establish, maintain, and reactivate from experimental latency in a manner comparable with parental virus, but major histocompatibility complex class II levels increased significantl…

Human cytomegalovirusCD4-Positive T-LymphocytesIsoantigensMyeloidGenes Viralmedicine.medical_treatmentImmunologyPopulationCytomegalovirusDown-RegulationBiologyIn Vitro Techniquesmedicine.disease_causeBiochemistryAutoantigensHerpesviridaeVirusImmune systemmedicineHumansProgenitor celleducationMyeloid Progenitor Cellseducation.field_of_studyHistocompatibility Antigens Class IICell BiologyHematologymedicine.diseaseVirologyVirus LatencyCytokinemedicine.anatomical_structureImmunologyCytomegalovirus InfectionsHost-Pathogen InteractionsGene DeletionBlood
researchProduct

Immune effects of 5-fluorouracil

2012

Cytotoxic anticancer drugs can promote antitumor immune responses. The anticancer activity of 5-fluorouracil (5FU) relies on the restoration of T-cell immunity following the elimination of myeloid-derived suppressor cells (MDSCs). We have recently discovered that the 5FU-driven activation of the NLRP3 inflammasome in MDSCs promotes tumor angiogenesis by eliciting TH17 responses that compromise anticancer immunity. This underscores the need to combine 5-FU with NLRP3 inhibitors to prevent tumor progression.

IL1business.industryImmunologychemical and pharmacologic phenomenaInflammasomemyeloid derived suppressor cellsfluorouracillaw.inventionImmune systemNLRP3OncologyinflammasomelawTumor progressionImmunityFluorouracilImmunologyMyeloid-derived Suppressor CellmedicineImmunology and AllergyCytotoxic T cellSuppressorbusinessAuthor's Viewmedicine.drugOncoImmunology
researchProduct

AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations

2005

Activating mutations of Flt3 are found in approximately one third of patients with acute myeloid leukemia (AML) and are an attractive drug target. Two classes of Flt3 mutations occur: internal tandem duplications (ITDs) in the juxtamembrane and point mutations in the tyrosine kinase domain (TKD). We and others have shown that Flt3-ITD induced aberrant signaling including strong activation of signal transducer and activator of transcription 5 (STAT5) and repression of CCAAT/estradiol-binding protein α (c/EBPα) and Pu.1. Here, we compared the signaling properties of Flt3-ITD versus Flt3-TKD in myeloid progenitor cells. We demonstrate that Flt3-TKD mutations induced autonomous growth of 32D ce…

ImmunologyApoptosisBiologymedicine.disease_causeBiochemistryCell Linefluids and secretionsProto-Oncogene Proteinshemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansPoint MutationMyeloid CellsPhosphorylationProtein kinase BProtein kinase CMutationPoint mutationAutophosphorylationIntracellular Signaling Peptides and ProteinsReceptor Protein-Tyrosine Kinaseshemic and immune systemsCell BiologyHematologyMilk ProteinsStaurosporineMolecular biologyProtein Structure TertiaryDNA-Binding ProteinsMuridaefms-Like Tyrosine Kinase 3Leukemia MyeloidTandem Repeat SequencesAcute Diseaseembryonic structuresFms-Like Tyrosine Kinase 3Mutagenesis Site-DirectedTrans-ActivatorsSignal transductionTyrosine kinaseSignal TransductionTranscription FactorsBlood
researchProduct

Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

2005

Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is unclear but is of major significance for the development of future therapeutic strategies. We searched for mechanisms of resistance in 6 patients with AML who had relapses upon PKC412 treatment. In an …

ImmunologyMutation MissenseBiologyBiochemistrychemistry.chemical_compoundIn vivoRecurrencehemic and lymphatic diseasesHumansProtein Kinase InhibitorsProtein Kinase CQuizartinibKinaseMyeloid leukemiaCell BiologyHematologyProtein-Tyrosine KinasesStaurosporineEnzyme ActivationProtein kinase domainchemistryfms-Like Tyrosine Kinase 3Drug Resistance NeoplasmLeukemia MyeloidFms-Like Tyrosine Kinase 3Acute DiseaseCancer researchTyrosine kinaseCrenolanibBlood
researchProduct

miR-155: On the Crosstalk Between Inflammation and Cancer

2009

MicroRNAs are short non-coding RNAs that posttranscriptionally modulate the expression of multiple target genes and are thus implicated in a wide array of cellular and developmental processes. miR-155 is processed from BIC, a non-coding transcript highly expressed in both activated B and T cells and in monocytes/macrophages. miR-155 levels change dynamically during both hematopoietic lineage differentiation and the course of the immune response. Different mouse models developed recently indicate that miR-155 plays a critical role during hematopoiesis and regulates lymphocyte homeostasis and tolerance. A moderate increase of miR-155 levels is observed in many types of malignancies of B cell …

InflammationRegulation of gene expressionInnate immune systemMyeloidImmunologyGene ExpressionBiologyAcquired immune systemCell biologymiR-155MiceMicroRNAsmedicine.anatomical_structureImmune systemGene Expression RegulationNeoplasmsLymphocyte homeostasisImmunologymedicineAnimalsHumansImmunology and AllergyB cellInternational Reviews of Immunology
researchProduct

Candida albicansstimulatesin vivodifferentiation of haematopoietic stem and progenitor cells towards macrophages by a TLR2-dependent signalling

2013

Toll-like receptors (TLRs) are expressed by haematopoietic stem and progenitor cells (HSPCs), and may play a role in haematopoiesis in response to pathogens during infection. We have previously demonstrated that (i) inactivated yeasts of Candida albicans induce in vitro differentiation of HSPCs towards the myeloid lineage, and (ii) soluble TLR agonists induce in vivo their differentiation towards macrophages. In this work, using an in vivo model of HSPCs transplantation, we report for the first time that HSPCs sense C. albicans in vivo and subsequently are directed to produce macrophages by a TLR2-dependent signalling. Purified lineage-negative cells (Lin(-)) from bone marrow of C57BL/6 mic…

Innate immune systemMyeloidCellular differentiationImmunologyBiologyMicrobiologyCell biologyTransplantationHaematopoiesisTLR2medicine.anatomical_structureVirologyImmunologymedicineBone marrowProgenitor cellCellular Microbiology
researchProduct