Search results for " Immunology"

showing 10 items of 1841 documents

Visualizing Leukocyte Rolling and Adhesion in Angiotensin II-Infused Mice: Techniques and Pitfalls

2018

Epifluorescence intravital video microscopy (IVM) of blood vessels is an established method to evaluate the activation of immune cells and their ability to role and adhere to the endothelial layer. Visualization of circulating cells by injection of fluorescent dyes or fluorophore-coupled antibodies is commonly used. Alternatively, fluorescent reporter mice can be used. Interactions of leukocytes, in particular lysozyme M+ (LysM+) monocytes, with the vessel wall play pivotal roles in promoting vascular dysfunction and arterial hypertension. We here present the technique to visualize and quantify leukocyte rolling and adhesion in carotid arteries in angiotensin II (AngII)-induced hypertension…

0301 basic medicineMaleEndotheliumendotheliumGeneral Chemical EngineeringImmunologyLeukocyte RollingMice TransgenicMonocytesGeneral Biochemistry Genetics and Molecular BiologyGreen fluorescent protein03 medical and health scienceschemistry.chemical_compoundMiceintravital microscopymedicineacridine orangeCell AdhesionLeukocytesAnimalsLeukocyte RollingCell adhesionGeneral Immunology and Microbiologycarotid arteryAngiotensin IIGeneral NeuroscienceAcridine orangeAngiotensin IICell biologyIssue 131030104 developmental biologymedicine.anatomical_structureCarotid ArterieschemistryHypertensioncardiovascular systemdouble-fluorescent Cre reporter mouseCell activationIntravital microscopyJournal of Visualized Experiments
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Interleukin-25 Axis Is Involved in the Pathogenesis of Human Primary and Experimental Murine Sjögren's Syndrome

2018

Objective To investigate the role of the interleukin-25 (IL-25)/IL-17 receptor B (IL-17RB) axis in experimental Sjogren's syndrome (SS) and in patients with primary SS and primary SS-associated lymphoma. Methods Expression of IL-25, IL-17RB, IL-17B, and tumor necrosis factor receptor-associated factor 6 (TRAF6) was analyzed on minor salivary gland (SG) samples from patients with primary SS and on parotid gland samples from patients with primary SS-associated B cell non-Hodgkin's lymphoma (NHL). IL-17RB expression and the frequencies of natural group 2 innate lymphoid cells (ILC2s), inflammatory ILC2s, and M2-polarized macrophages were assessed by flow cytometry in SG mononuclear cells and p…

0301 basic medicineMaleLymphomaMacrophageImmunologyPeripheral blood mononuclear cellSalivary GlandSalivary GlandsFlow cytometry03 medical and health sciencesMice0302 clinical medicineRheumatologyInterleukin 25AnimalsHumansMedicineImmunology and AllergyLymphocytesB cellAgedReceptors Interleukin-17medicine.diagnostic_testbusiness.industryAnimalMacrophagesInnate lymphoid cellInterleukin-17Middle Agedmedicine.diseaseImmunity InnateLymphomaSettore MED/16 - Reumatologia030104 developmental biologymedicine.anatomical_structureSjogren's SyndromeImmunologyImmunology and Allergy; Rheumatology; ImmunologyLeukocytes MononuclearRituximabTumor necrosis factor alphaFemaleLymphocytebusiness030215 immunologymedicine.drugHuman
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Dopamine neurons drive fear extinction learning by signaling the omission of expected aversive outcomes

2018

Extinction of fear responses is critical for adaptive behavior and deficits in this form of safety learning are hallmark of anxiety disorders. However, the neuronal mechanisms that initiate extinction learning are largely unknown. Here we show, using single-unit electrophysiology and cell-type specific fiber photometry, that dopamine neurons in the ventral tegmental area (VTA) are activated by the omission of the aversive unconditioned stimulus (US) during fear extinction. This dopamine signal occurred specifically during the beginning of extinction when the US omission is unexpected, and correlated strongly with extinction learning. Furthermore, temporally-specific optogenetic inhibition o…

0301 basic medicineMaleMouseExtinction PsychologicalPhotometry0302 clinical medicineFear conditioningBiology (General)extinctionGeneral NeuroscienceQRElectroencephalographyGeneral MedicineFearmusculoskeletal systemhumanitiesVentral tegmental areamedicine.anatomical_structureMedicineAnxietymedicine.symptomdopaminePsychologygeographic locationsmedicine.drugResearch ArticleQH301-705.5ScienceOptogeneticsUnconditioned stimulussafety learningGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesextinction ; fear conditioning ; safety learning ; dopamineDopaminemedicineAvoidance LearningAnimalsLearningddc:610General Immunology and MicrobiologyDopaminergic NeuronsVentral Tegmental AreaExtinction (psychology)social sciencesfear conditioningMice Inbred C57BLOptogeneticsElectrophysiology030104 developmental biologyNeuroscience030217 neurology & neurosurgeryNeuroscience
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Oligodendrocytes support axonal transport and maintenance via exosome secretion

2020

Neurons extend long axons that require maintenance and are susceptible to degeneration. Long-term integrity of axons depends on intrinsic mechanisms including axonal transport and extrinsic support from adjacent glial cells. The mechanisms of support provided by myelinating oligodendrocytes to underlying axons are only partly understood. Oligodendrocytes release extracellular vesicles (EVs) with properties of exosomes, which upon delivery to neurons improve neuronal viability in vitro. Here, we show that oligodendroglial exosome secretion is impaired in 2 mouse mutants exhibiting secondary axonal degeneration due to oligodendrocyte-specific gene defects. Wild-type oligodendroglial exosomes …

0301 basic medicineMaleMutantHippocampusCentrifugationExosomesAxonal TransportHippocampusMass SpectrometryAnalytical ChemistryMiceMyelin0302 clinical medicineNerve FibersSpectrum Analysis TechniquesAnimal CellsMedicine and Health SciencesBiology (General)Myelin SheathNeuronsLiquid ChromatographyGeneral NeuroscienceChromatographic TechniquesBrainCell biologyChemistrySeparation ProcessesOligodendrogliamedicine.anatomical_structureCell ProcessesPhysical SciencesFemaleCellular TypesCellular Structures and OrganellesAnatomyGeneral Agricultural and Biological SciencesNeurogliaResearch ArticleSignal TransductionMaintenanceQH301-705.5Liquid Chromatography-Mass SpectrometryBiologyResearch and Analysis MethodsExosomeGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesExtracellular VesiclesmedicineAnimalsHumansSecretionVesiclesGeneral Immunology and MicrobiologyWild typeBiology and Life SciencesCell BiologyIn vitroAxonsMicrovesiclesMice Inbred C57BL030104 developmental biologyHEK293 Cellsnervous systemCellular NeuroscienceAxoplasmic transportNeuronUltracentrifugation030217 neurology & neurosurgeryNeuroscience
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Different behavior of myeloperoxidase in two rodent amoebic liver abscess models.

2016

The protozoan Entamoeba histolytica is the etiological agent of amoebiasis, which can spread to the liver and form amoebic liver abscesses. Histological studies conducted with resistant and susceptible models of amoebic liver abscesses (ALAs) have established that neutrophils are the first cells to contact invasive amoebae at the lesion site. Myeloperoxidase is the most abundant enzyme secreted by neutrophils. It uses hydrogen peroxide secreted by the same cells to oxidize chloride ions and produce hypochlorous acid, which is the most efficient microbicidal system of neutrophils. In a previous report, our group demonstrated that myeloperoxidase presents amoebicidal activity in vitro. The ai…

0301 basic medicineMalePathologyNeutrophilslcsh:MedicineGene ExpressionPathology and Laboratory MedicineWhite Blood Cells0302 clinical medicineAnimal CellsCricetinaeMedicine and Health SciencesAmoebaslcsh:ScienceImmune ResponseDisease ResistanceMammalsProtozoansMice Inbred BALB CMultidisciplinaryAmoebic liver abscessbiologyChemistryAnimal ModelsLiverExperimental Organism SystemsMyeloperoxidaseHost-Pathogen InteractionsVertebratesLiver Abscess AmebicHamstersmedicine.symptomCellular TypesResearch Articlemedicine.medical_specialtyImmune CellsImmunologyMouse ModelsResearch and Analysis MethodsRodentsMicrobiologyLesionEntamoeba Histolytica03 medical and health sciencesEntamoeba histolyticaModel OrganismsSigns and SymptomsIn vivoDiagnostic MedicineParasite GroupsmedicineGeneticsAnimalsAmoebiasisTrophozoitesPeroxidaseInflammationBlood Cellslcsh:ROrganismsBiology and Life SciencesCell Biologybiology.organism_classificationmedicine.diseaseIn vitroParasitic ProtozoansDisease Models Animal030104 developmental biologyAmniotesbiology.proteinlcsh:QParasitologyLeukocyte ElastaseApicomplexa030215 immunologyLiver abscessPloS one
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miRNA92a targets KLF2 and the phosphatase PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity.

2016

Aberrant immune activation mediated by T effector cell populations is pivotal in the onset of autoimmunity in type 1 diabetes (T1D). T follicular helper (TFH) cells are essential in the induction of high-affinity antibodies, and their precursor memory compartment circulates in the blood. The role of TFH precursors in the onset of islet autoimmunity and signaling pathways regulating their differentiation is incompletely understood. Here, we provide direct evidence that during onset of islet autoimmunity, the insulin-specific target T-cell population is enriched with a C-X-C chemokine receptor type 5 (CXCR5)(+)CD4(+) TFH precursor phenotype. During onset of islet autoimmunity, the frequency o…

0301 basic medicineMaleReceptors CXCR5endocrine systemAdolescentPopulationPrimary Cell CultureKruppel-Like Transcription FactorsAutoimmunityMice TransgenicNodBiologymedicine.disease_causeCXCR5Autoimmunity03 medical and health sciencesIslets of LangerhansMicePhosphatidylinositol 3-Kinases0302 clinical medicineMice Inbred NODmedicineAnimalsHumansIL-2 receptorKlf2 ; Pten-pi3k Signaling ; T Follicular Helper Cells ; Mirna92a ; Type 1 DiabeteseducationChildPI3K/AKT/mTOR pathwayNOD miceAutoantibodiesgeographyeducation.field_of_studyMultidisciplinarygeography.geographical_feature_categoryForkhead Box Protein O1PTEN PhosphohydrolaseAntagomirsT-Lymphocytes Helper-InducerIsletMicroRNAs030104 developmental biologyDiabetes Mellitus Type 1Gene Expression RegulationImmunologyCancer researchFemale030215 immunologySignal Transduction
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Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
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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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Vitellogenin-like A–associated shifts in social cue responsiveness regulate behavioral task specialization in an ant

2018

Division of labor and task specialization explain the success of human and insect societies. Social insect colonies are characterized by division of labor, with workers specializing in brood care early and foraging later in life. Theory posits that this task switching requires shifts in responsiveness to task-related cues, yet experimental evidence is weak. Here, we show that a Vitellogenin (Vg) ortholog identified in an RNAseq study on the ant T. longispinosus is involved in this process: using phylogenetic analyses of Vg and Vg-like genes, we firstly show that this candidate gene does not cluster with the intensively studied honey bee Vg but falls into a separate Vg-like A cluster. Second…

0301 basic medicineMaleTask switchingAgingFat BodySocial SciencesGene ExpressionGenes InsectBiochemistryFatsVitellogeninsSociologyGene Regulatory NetworksForagingBiology (General)reproductive and urinary physiologyPhylogenyAnimal BehaviorBehavior AnimalGeneral NeuroscienceEukaryotaBeesLipidsANTInsectsAnimal SocialityGene Knockdown TechniquesMultigene FamilySocial SystemsInsect ProteinsFemaleCuesGeneral Agricultural and Biological SciencesHoney BeesDivision of labourResearch ArticleArthropodaQH301-705.5ForagingBiologyModels BiologicalGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesSpecies Specificityddc:570Specialization (functional)GeneticsAnimalsSocial BehaviorBehaviorGeneral Immunology and MicrobiologyAntsfungiOrganismsBiology and Life SciencesHoney beeSocial cueInvertebratesHymenopteraBrood030104 developmental biologyEvolutionary biologyZoologyPLoS Biology
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