Search results for " immune system"

showing 10 items of 893 documents

Phenotypic and functional characterization of neutrophils and monocytes from patients with myelodysplastic syndrome by flow cytometry.

2016

Myelodysplastic syndrome (MDS) is a clonal stem cell disorder frequently associated with inefficient granulopoiesis showing dysplastic polymorphonuclear neutrophils (PMNs). To assess PMN functionality in MDS in a clinical routine setting, 30 MDS patients and ten healthy volunteers were analyzed for PMN and monocyte phenotype and function (degranulation, CD62L shedding, oxidative burst and phagocytosis) upon stimulation with lipopolysaccharide by multi-color flow cytometry (MCFC). Our data show a heterogeneous pattern for CD66, CD16 and CD64 expression on PMNs of MDS patients. CD62L shedding rate and CD66 degranulation were reduced. Interestingly, we detected correlations between the WHO ada…

0301 basic medicineMaleCell DegranulationNeutrophilsImmunologyCell SeparationBiologyGranulopoiesisCell DegranulationMonocytesFlow cytometryImmunophenotyping03 medical and health sciences0302 clinical medicineMonitoring ImmunologicmedicineHumans610 Medicine & healthAgedMonitoring PhysiologicCD64Aged 80 and overCD11b Antigenmedicine.diagnostic_testMyelodysplastic syndromesMonocyteReceptors IgGDegranulationhemic and immune systemsMiddle Agedmedicine.diseaseFlow CytometryPrognosis030104 developmental biologymedicine.anatomical_structureInternational Prognostic Scoring SystemMyelodysplastic SyndromesImmunologyFemale030215 immunologyCellular immunology
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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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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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The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

2020

The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Fu…

0301 basic medicineMaleGene Expression030204 cardiovascular system & hematologyvon Willebrand factorlcsh:Chemistrychemistry.chemical_compoundMice0302 clinical medicinePlateletToll-like receptor-2lcsh:QH301-705.5SpectroscopyMice KnockoutbiologyChemistryBrief ReportαIIbβ3General MedicineArteriesComputer Science ApplicationsCell biologyAdenosine DiphosphatePlatelet Glycoprotein GPIb-IX Complexgerm-freeplateletsFemaleType I collagenBlood PlateletsIntegrinPrimary Cell CulturePlatelet Glycoprotein GPIIb-IIIa ComplexCatalysisCollagen Type IInorganic Chemistry03 medical and health sciencesVon Willebrand factormedicineCell AdhesionmicrobiotaAnimalsGerm-Free LifeHumansPhysical and Theoretical ChemistryThrombusSymbiosisMolecular Biologyα<sub>IIb</sub>β<sub>3</sub>Innate immune systemOrganic ChemistryThrombosismedicine.diseaseImmunity InnateToll-Like Receptor 2Gastrointestinal MicrobiomeMice Inbred C57BLAdenosine diphosphateTLR2030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinInternational Journal of Molecular Sciences
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Disease severity in patients with visceral leishmaniasis is not altered by co-infection with intestinal parasites

2017

Visceral leishmaniasis (VL) is a neglected tropical disease that affects the poorest communities and can cause substantial morbidity and mortality. Visceral leishmaniasis is characterized by the presence of Leishmania parasites in the spleen, liver and bone marrow, hepatosplenomegaly, pancytopenia, prolonged fever, systemic inflammation and low body mass index (BMI). The factors impacting on the severity of VL are poorly characterized. Here we performed a cross-sectional study to assess whether co-infection of VL patients with intestinal parasites influences disease severity, assessed with clinical and haematological data, inflammation, cytokine profiles and BMI. Data from VL patients was s…

0301 basic medicineMaleIMPACTPhysiologyHepatosplenomegalySystemic inflammationPathology and Laboratory MedicineTHERAPYSeverity of Illness IndexBody Mass Index0302 clinical medicineIntestinal ParasitesBone MarrowZoonosesImmune PhysiologyMedicine and Health SciencesIntestinal Diseases ParasiticHELMINTH INFECTIONSLeishmaniasisImmune ResponseInnate Immune SystembiologyCoinfectionlcsh:Public aspects of medicineASCARIASIS11 Medical And Health SciencesHematologyPancytopenia3. Good healthInfectious DiseasesCytokinesLeishmaniasis Visceralmedicine.symptomLife Sciences & BiomedicineHepatomegalyResearch ArticleNeglected Tropical DiseasesAdultlcsh:Arctic medicine. Tropical medicineAdolescentlcsh:RC955-962030231 tropical medicineImmunology03 medical and health sciencesYoung AdultSigns and SymptomsDONOVANIDiagnostic MedicineTropical MedicineHOOKWORMSeverity of illnessmedicineParasitic DiseasesAnimalsHumansParasitesInflammationScience & TechnologyProtozoan InfectionsINTERFERON-GAMMAbusiness.industryPublic Health Environmental and Occupational HealthTropical diseaseBiology and Life SciencesLeishmaniasislcsh:RA1-127006 Biological SciencesMolecular DevelopmentINTERLEUKIN-10Leishmaniabiology.organism_classificationmedicine.diseaseTropical Diseases030104 developmental biologyVisceral leishmaniasisCross-Sectional StudiesLogistic ModelsCase-Control StudiesCo-InfectionsImmune SystemImmunologySplenomegalyUNDERNUTRITIONParasitologyEthiopiabusinessParasitic Intestinal DiseasesSpleenDevelopmental Biology
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Plasmacytoid dendritic cells promote systemic sclerosis with a key role for TLR8

2018

Systemic sclerosis (SSc) is a multisystem life-threatening fibrosing disorder that lacks effective treatment. The link between the inflammation observed in organs such as the skin and profibrotic mechanisms is not well understood. The plasmacytoid dendritic cell (pDC) is a key cell type mediating Toll-like receptor (TLR)-induced inflammation in autoimmune disease patients, including lupus and skin diseases with interface dermatitis. However, the role of pDCs in fibrosis is less clear. We show that pDCs infiltrate the skin of SSc patients and are chronically activated, leading to secretion of interferon-α (IFN-α) and CXCL4, which are both hallmarks of the disease. We demonstrate that the s…

0301 basic medicineMaleInflammationPlasmacytoid dendritic cellPlatelet Factor 4SclerodermaArticlePathogenesis03 medical and health sciencesBleomycinMice0302 clinical medicineFibrosismedicineAnimalsHumansSkin030203 arthritis & rheumatologyAutoimmune diseaseSystemic lupus erythematosusScleroderma Systemicintegumentary systembusiness.industryMedicine (all)Interferon-alphahemic and immune systemsGeneral MedicineTLR7Dendritic CellsMiddle Agedmedicine.diseaseFibrosisDisease Models Animal030104 developmental biologyToll-Like Receptor 7Toll-Like Receptor 8ImmunologyFemalemedicine.symptombusinessSignal Transduction
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Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study

2017

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic …

0301 basic medicineMaleLymphocyteReceptor expressionProgrammed Cell Death 1 Receptorlcsh:MedicineCytomegalovirusGene ExpressionArtificial Gene Amplification and ExtensionPathology and Laboratory MedicineImmune ReceptorsBiochemistryPolymerase Chain ReactionMonocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesAnimal CellsT-Lymphocyte SubsetsMedicine and Health SciencesLymphocyteslcsh:ScienceAged 80 and overMultidisciplinaryImmune System ProteinsT CellsMiddle AgedAcquired immune systemFlow CytometryPrognosisShock Septicmedicine.anatomical_structurePhenotypeSpectrophotometryShock (circulatory)Cytomegalovirus InfectionsFemaleCytophotometrymedicine.symptomCellular TypesResearch ArticleSignal TransductionT cellImmune CellsImmunologyReceptors Antigen T-CellBiologyResearch and Analysis MethodsMicrobiologyImmunophenotypingSepsis03 medical and health sciencesImmune systemSigns and SymptomsDiagnostic MedicineSepsisVirologymedicineHumansMolecular Biology TechniquesMolecular BiologyAgedBlood CellsSeptic shocklcsh:RBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyHLA-DR Antigensmedicine.diseaseViral ReplicationT Cell Receptors030104 developmental biologyCase-Control StudiesImmunologylcsh:QBiomarkersPLoS ONE
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Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

2016

The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival and activation are essential for inflammation resolution and contributes directly to the pathogenesis of many infectious and inflammatory conditions. The aim of this study was to investigate the effect of marathon races on surface molecules related to neutrophil adhesion and extrinsic apoptosis pathway and its association with inflammatory markers. We evaluated 23 trained male runners at the Sao Paulo International Marathon 2013. The following components were measured: hematological and inflammatory mediators, muscle damage markers, and neutrophil function. The maratho…

0301 basic medicineMaleNeutrophilsPhysiologylcsh:MedicineApoptosisDNA fragmentationPathology and Laboratory MedicineBiochemistryNeutrophil ActivationRunningPathogenesischemistry.chemical_compoundWhite Blood CellsLeukocyte Count0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinarybiologyCell DeathInterleukinHematologyFas receptorBody FluidsNucleic acidsBloodHematocritCell ProcessesAntigens SurfaceCytokinesTumor necrosis factor alphamedicine.symptomCellular TypesAnatomyInflammation MediatorsResearch ArticleAdultCell SurvivalImmune CellseducationImmunologyInflammation03 medical and health sciencesSigns and SymptomsDiagnostic MedicineLactate dehydrogenasemedicineGeneticsHumansLeukocyte RollingHemoglobinInflammationBlood Cellsbusiness.industrylcsh:RBiology and Life SciencesProteins030229 sport sciencesCell BiologyDNAMolecular DevelopmentBlood Counts030104 developmental biologychemistryApoptosisImmune SystemImmunologybiology.proteinCreatine kinaselcsh:Qbusinesshuman activitiesDevelopmental BiologyPLoS ONE
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Fasciola hepatica reinfection potentiates a mixed Th1/Th2/Th17/Treg response and correlates with the clinical phenotypes of anemia.

2016

Background: Fascioliasis is a severe zoonotic disease of worldwide extension caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm and anemia is the main sign. Herein, the profile of the Th1/Th2/Th17/Treg expression levels is analyzed after reinfection, correlating them with their corresponding hematological biomarkers of morbidity. Methodology/Principal findings: The experimental design reproduces the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 8 weeks (R8), and at 12 weeks (R12), and negative control rats. In a cross-sect…

0301 basic medicineMalePhysiologymedicine.medical_treatmentSnailslcsh:MedicineGene ExpressionImmune PhysiologyGene expressionMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsImmunosuppressionEBI3AnemiaForkhead Transcription FactorsHematologyThymusInterleukin-10Interleukin 10medicine.anatomical_structureHelminth InfectionsCytokinesResearch ArticleNeglected Tropical DiseasesFascioliasisImmunologychemical and pharmacologic phenomenaSpleenBiologyTransforming Growth Factor beta103 medical and health sciencesImmune systemTh2 CellsGeneticsParasitic DiseasesmedicineFasciola hepaticaAnimalsRats WistarCell ProliferationInterleukinslcsh:RBiology and Life SciencesMolecular DevelopmentFasciola hepaticaTh1 CellsTropical Diseasesbiology.organism_classificationRats030104 developmental biologyCross-Sectional StudiesImmune SystemImmunologyTh17 Cellslcsh:QSpleenDevelopmental Biology
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Mast cells are associated with the onset and progression of celiac disease

2017

Background Celiac disease (CD) is an immune-mediated disorder characterized by an accumulation of immune cells in the duodenal mucosa as a consequence of both adaptive and innate immune responses to undigested gliadin peptides. Mast cells (MCs) are innate immune cells that are a major source of costimulatory signals and inflammatory mediators in the intestinal mucosa. Although MCs have previously been associated with CD, functional studies have never been performed. Objective We aimed at evaluating the role of MCs in the pathogenesis of CD. Methods Intestinal biopsy specimens of patients with CD were scored according to the Marsh classification and characterized for leukocyte infiltration a…

0301 basic medicineMaleSettore MED/09 - Medicina InternaImmunologygliadin immunologyFluorescent Antibody TechniqueBiologyCell DegranulationGliadinProinflammatory cytokinePathogenesis03 medical and health sciencesMice0302 clinical medicineImmune systemIntestinal mucosamedicineImmunology and AllergyAnimalsHumansCeliac diseaseMast CellsIntestinal Mucosap31-43 fragmentToll-like receptorInnate immune systemCeliac disease; gliadin immunology; mast cell; p31-43 fragment; mast cellFOXP3Mast cellImmunohistochemistryhumanitiesPeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyDisease ProgressionFemalemast cell
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