Search results for "Lymph"

showing 10 items of 4590 documents

CD19 Isoforms Enabling Resistance to CART-19 Immunotherapy Are Expressed in B-ALL Patients at Initial Diagnosis.

2017

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0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT-LymphocytesEpitopes T-LymphocyteT-Cell Antigen Receptor SpecificityImmunotherapy AdoptiveEpitopeCohort StudiesExon0302 clinical medicineimmune system diseasesImmunology and AllergyMedicineProtein IsoformsChildAged 80 and overbiologyCD19CART-19B-ALLMiddle AgedPrecursor Cell Lymphoblastic Leukemia-Lymphomaepitope-lossmedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisChild PreschoolComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleClone (B-cell biology)Gene isoformAdultAdolescentRecombinant Fusion ProteinsImmunologyAntigens CD19Receptors Antigen T-CellCancer VaccinesCD1903 medical and health sciencesYoung AdultAntigenHumansAgedPharmacologybusiness.industryInfant NewbornisoformsInfantImmunotherapy030104 developmental biologyImmunologybiology.proteinClinical StudyTumor EscapeBone marrowbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure.

2017

Hypertension represents a major cardiovascular risk factor. The pathophysiology of increased blood pressure (BP) is not yet completely understood. Transcriptome profiling offers possibilities to uncover genetics effects on BP. Based on 2 populations including 2549 individuals, a meta-analyses of monocytic transcriptome-wide profiles were performed to identify transcripts associated with BP. Replication was performed in 2 independent studies of whole-blood transcriptome data including 1990 individuals. For identified candidate genes, a direct link between long-term changes in BP and gene expression over time and by treatment with BP-lowering therapy was assessed. The predictive value of pro…

0301 basic medicineMaleCandidate geneGene ExpressionGenome-wide association studyBlood Pressure030204 cardiovascular system & hematologyCardiorespiratory Medicine and HaematologyCardiovascularLMNATranscriptome0302 clinical medicineRisk FactorsCEBPAGene expression2.1 Biological and endogenous factorsAetiologyGeneticsMyelin and Lymphocyte-Associated Proteolipid ProteinsBlood Pressure ; Gene Expression ; Genome-wide Association Study ; Hypertension ; Transcriptomeblood pressureGenomicsSingle NucleotideLIM Domain Proteinsblood pressure; gene expression; genome-wide association study; hypertension; transcriptomeStrokeHeart DiseaseHypertensionPublic Health and Health ServicesBiomarker (medicine)FemaleEssential HypertensionPoly(ADP-ribose) PolymerasesBiotechnologyAdulthypertensionClinical SciencesNucleoside Transport ProteinsBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesClinical ResearchInternal MedicineGeneticsHumansPolymorphismgenome-wide association studyGene Expression ProfilingHuman GenomeBlood Pressure DeterminationGene expression profiling030104 developmental biologyGood Health and Well BeingCardiovascular System & Hematologygene expressionCCAAT-Enhancer-Binding ProteinsCarrier ProteinstranscriptomeTranscription Factors
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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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IFI16 reduced expression is correlated with unfavorable outcome in chronic lymphocytic leukemia.

2017

Chronic lymphocytic leukemia (CLL) is the most common leukemia in adults. Its clinical course is typically indolent; however, based on a series of pathobiological, clinical, genetic, and phenotypic parameters, patient survival varies from less than 5 to more than 20 years. In this paper, we show for the first time that the expression of the interferon-inducible DNA sensor IFI16, a member of the PYHIN protein family involved in proliferation inhibition and apoptosis regulation, is associated with the clinical outcome in CLL. We studied 99 CLLs cases by immunohistochemistry and 10 CLLs cases by gene expression profiling. We found quite variable degrees of IFI16 expression among CLLs cases. No…

0301 basic medicineMaleChronic lymphocytic leukemiaGene Expressionhemic and lymphatic diseasesGene expression80 and overImmunology and AllergyChronicNuclear ProteinCD20Aged 80 and overLeukemiaMembrane GlycoproteinsZAP-70 Protein-Tyrosine KinasebiologyZAP70Nuclear ProteinsGeneral MedicineMiddle AgedPhenotypeImmunohistochemistryLymphocyticchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; Adult; Aged; Aged 80 and over; Antigens CD38; Female; Gene Expression Profiling; Humans; Immunohistochemistry; Leukemia Lymphocytic Chronic B-Cell; Male; Membrane Glycoproteins; Middle Aged; Nuclear Proteins; Phosphoproteins; Treatment Outcome; Young Adult; ZAP-70 Protein-Tyrosine Kinase; Gene Expression; Immunology and Allergy; 2734; Microbiology (medical)LeukemiaTreatment OutcomePhosphoproteinimmunohistochemistryImmunohistochemistryZAP70FemaleMembrane GlycoproteinprognosiHumanMicrobiology (medical)Adult2734IFI16; ZAP70; chronic lymphocytic leukemia; gene expression; immunohistochemistry; prognosisNOPathology and Forensic Medicine03 medical and health sciencesYoung AdultmedicineHumansAntigensIFI16Agedbusiness.industryGene Expression ProfilingB-Cellchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; ADP-ribosyl Cyclase 1; Adult; Aged; Aged 80 and over; Female; Gene Expression Profiling; Humans; Immunohistochemistry; Leukemia Lymphocytic Chronic B-Cell; Male; Membrane Glycoproteins; Middle Aged; Nuclear Proteins; Phosphoproteins; Treatment Outcome; Young Adult; ZAP-70 Protein-Tyrosine Kinase; Gene Expression; 2734; Immunology and Allergy; Microbiology (medical)medicine.diseasePhosphoproteinsADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellGene expression profilingchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; Immunology and Allergy; 2734; Microbiology (medical)030104 developmental biologygene expressionCancer researchbiology.proteinchronic lymphocytic leukemiaprognosisbusinessCD38APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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Cohesin-dependent regulation of gene expression during differentiation is lost in cohesin-mutated myeloid malignancies.

2019

Cohesin complex disruption alters gene expression, and cohesin mutations are common in myeloid neoplasia, suggesting a critical role in hematopoiesis. Here, we explore cohesin dynamics and regulation of hematopoietic stem cell homeostasis and differentiation. Cohesin binding increases at active regulatory elements only during erythroid differentiation. Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding at these elements and Etv6 interacts with cohesin at chromatin. Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound loci, but augments self-renewal programs. Together with corroborative findings in acute myeloid le…

0301 basic medicineMaleCohesin complexChromosomal Proteins Non-HistoneImmunologyGene DosageCell Cycle ProteinsBiologyRegulatory Sequences Nucleic AcidBiochemistryHistones03 medical and health sciences0302 clinical medicineNeoplasmshemic and lymphatic diseasesCell Line TumorBiomarkers TumorHumansTranscription factorRegulation of gene expressionHematopoietic stem cell homeostasisMyeloid NeoplasiaMyeloproliferative DisordersCohesinProto-Oncogene Proteins c-etsGene Expression Regulation LeukemicETS transcription factor familyMyeloid leukemiafood and beveragesCell BiologyHematologyHematopoietic Stem CellsCell biologyChromatinHematopoiesisRepressor Proteins030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMutationFemalesense organsbiological phenomena cell phenomena and immunityNeoplasm GradingBLOOD CommentaryProtein BindingBlood
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NKp46-expressing human gut-resident intraepithelial Vδ1 T cell subpopulation exhibits high antitumor activity against colorectal cancer

2019

γδ T cells account for a large fraction of human intestinal intraepithelial lymphocytes (IELs) endowed with potent anti-tumor activities. However, little is known about their origin, phenotype and clinical relevance in colorectal cancer (CRC). To determine γδ IEL gut-specificity, homing and functions, γδ T cells were purified from human healthy blood, lymph nodes, liver, skin, intestine either disease-free or affected by CRC or generated from thymic precursors. The constitutive expression of NKp46 specifically identifies a new subset of cytotoxic Vδ1 T cells representing the largest fraction of gut-resident IELs. The ontogeny and gut-tropism of NKp46pos/Vδ1 IELs depends both on distinctive …

0301 basic medicineMaleColorectal cancerImmunotherapy AdoptiveMice0302 clinical medicineSex Hormone-Binding GlobulinCytotoxic T cellAntigens LyIntestinal MucosaIntraepithelial LymphocytesInnate immunityAged 80 and overGastroenterologyAge FactorsReceptors Antigen T-Cell gamma-deltaGeneral MedicineMiddle AgedPhenotypemedicine.anatomical_structure030220 oncology & carcinogenesisDisease ProgressionFemaleColorectal NeoplasmsResearch ArticleAdultColonT cellImmunologyT cellsBiologydigestive systemColorectal cancer; Gastroenterology; Immunology; Innate immunity; T cells03 medical and health sciencesYoung AdultIleummedicineAnimalsHumansAgedNeoplasm StagingTumor microenvironmentInnate immune systemNatural Cytotoxicity Triggering Receptor 1medicine.diseaseColorectal cancer030104 developmental biologyCancer researchIntraepithelial lymphocyteHoming (hematopoietic)T-Lymphocytes Cytotoxic
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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

2020

Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, i…

0301 basic medicineMaleDendritic spineGeneral Physics and AstronomyHippocampal formationVARIANTSADULT NEUROGENESIS0302 clinical medicineCognitionhemic and lymphatic diseasesReceptors ErythropoietinHypoxialcsh:ScienceNEURONSMultidisciplinaryNeuronal PlasticityPyramidal CellsNeurogenesisQBrainCell DifferentiationHEMATOPOIETIC PROGENITOR CELLSFemalemedicine.symptomProto-Oncogene Proteins c-fosmedicine.drugEXPRESSIONScienceDendritic SpinesNeurogenesisModels NeurologicalBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesParacrine signallingPhysical Conditioning AnimalNeuroplasticitymedicineAnimalsHumansErythropoietinMEMORYCognitive neuroscienceGeneral ChemistryHypoxia (medical)RECOMBINANT-HUMAN-ERYTHROPOIETINCellular neuroscienceErythropoietin receptorMice Inbred C57BLMICE030104 developmental biologyErythropoietinPhysical EnduranceIDENTITYlcsh:QTranscriptomeNeuroscience030217 neurology & neurosurgeryGene Deletion
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Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome.

2021

Abstract Wiedemann-Steiner syndrome (WDSTS) is a rare genetic disorder including developmental delay/intellectual disability (DD/ID), hypertrichosis cubiti, short stature, and distinctive facial features, caused by mutation in KMT2A gene, which encodes a histone methyltransferase (H3K4) that regulates chromatin-mediated transcription. Different neurodevelopmental phenotypes have been described within the WDSTS spectrum, including a peculiar Autism Spectrum Disorder (ASDs) subtype in some affected individuals. Here, we report a 9-year-old Caucasian male found by next-generation panel sequencing to carry a novel heterozygous de novo KMT2A frameshift variant (NM_001197104.2:c.4433delG; p. Arg1…

0301 basic medicineMaleDevelopmental Disabilities030105 genetics & heredityBiologyFocal cortical dysplasiaPalilaliaFrameshift mutation03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumansChildFrameshift MutationGenetics (clinical)GeneticsCerebral CortexWiedemann-steiner syndrome.Genetic disorderHypertrichosis cubitiGeneral MedicineHistone-Lysine N-MethyltransferaseSyndromeKMT2ACortical dysplasiamedicine.diseasePalilaliaMalformations of Cortical Development030104 developmental biologyKMT2AWiedemann-Steiner syndromeAutism spectrum disorderbiology.proteinmedicine.symptomMyeloid-Lymphoid Leukemia ProteinEuropean journal of medical genetics
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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