Search results for "CX3C Chemokine Receptor 1"

showing 10 items of 10 documents

CNS-localized myeloid cells capture living invading T cells during neuroinflammation

2020

Using an in vivo real-time approach, the authors show that local myeloid cells remove early CNS-invading T cells via an engulfment pathway that is dependent on N-acetyl-D-glucosamine (GlcNAc) and lectin. These results reveal a novel capacity of myeloid cells to counteract neuroinflammation.

0301 basic medicineCentral Nervous SystemProgrammed cell deathCell signalingEncephalomyelitis Autoimmune ExperimentalCell SurvivalEncephalomyelitisT cellT-LymphocytesImmunologyInnate Immunity and InflammationCX3C Chemokine Receptor 1AutoimmunityReceptors Cell SurfaceCell CommunicationPhosphatidylserinesBiologyLymphocyte ActivationSeverity of Illness IndexArticle03 medical and health sciencesMice0302 clinical medicineNeuroinflammationPhagocytosisIn vivomedicineImmunology and AllergyAnimalsLectins C-TypeMyeloid CellsNeuroinflammationInflammationGlucosamineCell DeathExperimental autoimmune encephalomyelitismedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding LectinsTh17 Cells030217 neurology & neurosurgeryEx vivoMannose ReceptorThe Journal of Experimental Medicine
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Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Polymorphisms within the ARNT2 and CX3CR1 Genes Are Associated with the Risk of Developing Invasive Aspergillosis.

2020

Invasive aspergillosis (IA) is a life-threatening infection that affects an increasing number of patients undergoing chemotherapy or allo-transplantation, and recent studies have shown that genetic factors contribute to disease susceptibility. In this two-stage, population-based, case-control study, we evaluated whether 7 potentially functional single nucleotide polymorphisms (SNPs) within the ARNT2 and CX3CR1 genes influence the risk of IA in high-risk hematological patients. We genotyped selected SNPs in a cohort of 500 hematological patients (103 of those had been diagnosed with proven or probable IA), and we evaluated their association with the risk of developing IA. The association of …

0301 basic medicinehost immunityGenotype030106 microbiologyImmunologyPopulationCX3C Chemokine Receptor 1Single-nucleotide polymorphismARNT2 ; CX3CR1 ; genetic susceptibility; host immunity; invasive aspergillosisBiologyAspergillosisMicrobiologyPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesCX3CR1GenotypemedicineGenetic predispositionBasic Helix-Loop-Helix Transcription FactorsHumansGenetic Predisposition to DiseaseARNT2AlleleeducationInvasive Pulmonary Aspergillosiseducation.field_of_studyinvasive aspergillosisHaplotypeAryl Hydrocarbon Receptor Nuclear TranslocatorPCRAGA Study Groupmedicine.diseaseHematologic Diseases3. Good healthSettore MED/15 - MALATTIE DEL SANGUE030104 developmental biologyInfectious DiseasesAspergillusCase-Control StudiesExpression quantitative trait lociImmunologyParasitologygenetic susceptibility
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Proinflammatory CX3CR1+CD59+Tumor Necrosis Factor–Like Molecule 1A+Interleukin‐23+ Monocytes Are Expanded in Patients With Ankylosing Spondylitis and…

2018

Objective: Gut-derived innate lymphoid cell 3 (ILC3) has been shown to participate in the pathogenesis of ankylosing spondylitis (AS). CX3CR1+ mononuclear phagocytes (MNPs) have been demonstrated to modulate ILC3 function in the gut. This study was undertaken to investigate the role of proinflammatory CX3CR1+CD59+ MNPs in modulating ILC3 function in AS patients. Methods: MNP subsets in the blood of AS patients and controls were analyzed by flow cytometry. The presence of CX3CR1+CD59+ cells in tissue was confirmed by confocal microscopy. Expression of the proinflammatory chemokines CX3CL1 and CCL2 and decoy receptor 6 (DcR-6) was analyzed. Peripheral CX3CR1+CD59+ cells were cocultured with I…

AdultMale0301 basic medicineChemokineImmunologyPopulationCX3C Chemokine Receptor 1CD11cCD59 Antigenschemical and pharmacologic phenomenaCCL2Interleukin-23MonocytesProinflammatory cytokineFlow cytometry03 medical and health sciences0302 clinical medicineRheumatologymedicineHumansImmunology and AllergySpondylitis AnkylosingLymphocytesCX3CL1educationMononuclear Phagocyte System030203 arthritis & rheumatologyeducation.field_of_studybiologymedicine.diagnostic_testChemistryInnate lymphoid cellMiddle AgedImmunity Innate030104 developmental biologyReceptors Tumor Necrosis Factor Type ICase-Control Studiesbiology.proteinCancer researchFemaleArthritis & Rheumatology
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CX3CR1/CX3CL1 Axis Mediates Platelet–Leukocyte Adhesion to Arterial Endothelium in Younger Patients with a History of Idiopathic Deep Vein Thrombosis

2018

AbstractMechanisms linking deep vein thrombosis (DVT) and subclinical atherosclerosis and risk of cardiovascular events are poorly understood. The aim of this study was to investigate the potential impact of CX3CR1/CX3CL1 axis in DVT-associated endothelial dysfunction. The study included 22 patients (age: 37.5 ± 8.2 years) with a history of idiopathic DVT and without known cardiovascular risk factors and 23 aged-matched control subjects (age: 34 ± 7.8 years). Flow cytometry was used to evaluate peripheral markers of platelet activation, leukocyte immunophenotypes and CX3CR1/CX3CL1 expression in both groups. A flow chamber assay was employed to measure leukocyte arrest under dynamic conditio…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAdolescentEndotheliumCX3C Chemokine Receptor 1InflammationComorbidity030204 cardiovascular system & hematologyMonocytesImmunophenotypingYoung Adult03 medical and health sciencesPlatelet Adhesiveness0302 clinical medicineRisk FactorsPlatelet adhesivenessHuman Umbilical Vein Endothelial CellsLeukocytesmedicineHumansPlateletLymphocytescardiovascular diseasesPlatelet activationEndothelial dysfunctionSistema cardiovascularInflammationVenous ThrombosisChemokine CX3CL1Tumor Necrosis Factor-alphabusiness.industryEndothelial CellsHematologyMiddle AgedPlatelet Activationmedicine.diseaseThrombosis030104 developmental biologymedicine.anatomical_structureMicroscopy FluorescenceCase-Control StudiesFemaleEndothelium Vascularmedicine.symptombusinessPlatelet factor 4Thrombosis and Haemostasis
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A novel role of the CX3CR1/CX3CL1 system in the cross-talk between chronic lymphocytic leukemia cells and tumor microenvironment

2011

Several chemokines/chemokine receptors such as CCR7, CXCR4 and CXCR5 attract chronic lymphocytic leukemia (CLL) cells to specific microenvironments. Here we have investigated whether the CX(3)CR1/CX(3)CL1 axis is involved in the interaction of CLL with their microenvironment. CLL cells from 52 patients expressed surface CX(3)CR1 and CX(3)CL1 and released constitutively soluble CX(3)CL1. One third of these were attracted in vitro by soluble CX(3)CL1. CX(3)CL1-induced phosphorylation of PI3K, Erk1/2, p38, Akt and Src was involved in induction of CLL chemotaxis. Leukemic B cells upregulated CXCR4 upon incubation with CX(3)CL1 and this was paralleled by increased chemotaxis to CXCL12. Akt phosp…

AdultMalechemokines; chronic lymphocytic leukemia (CLL); nurselike cells (NLCs); tumor microenvironmentCancer ResearchChemokineStromal cellChronic lymphocytic leukemiaCX3C Chemokine Receptor 1Antigens Differentiation MyelomonocyticchemokinesC-C chemokine receptor type 7Cell Communicationnurselike cells (NLCs)Chemokine receptorAntigens CDimmune system diseaseshemic and lymphatic diseaseschronic lymphocytic leukemia (CLL)medicineHumanstumor microenvironmentPhosphorylationAgedAged 80 and overTumor microenvironmentbiologyChemokine CX3CL1ChemistryChemotaxisHematologyMiddle Agedmedicine.diseaseLeukemia Lymphocytic Chronic B-CellCX(3)CR1/CX(3)CL1 systemCX(3)CR1/CX(3)CL1 system; chronic lymphocytic leukemia.LeukemiaHaematopoiesisOncologychronic lymphocytic leukemia.Cancer researchbiology.proteinFemaleReceptors ChemokineLymph NodesProto-Oncogene Proteins c-aktSignal TransductionLeukemia
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Genetic Cell Ablation Reveals Clusters of Local Self-Renewing Microglia in the Mammalian Central Nervous System

2015

SummaryDuring early embryogenesis, microglia arise from yolk sac progenitors that populate the developing central nervous system (CNS), but how the tissue-resident macrophages are maintained throughout the organism’s lifespan still remains unclear. Here, we describe a system that allows specific, conditional ablation of microglia in adult mice. We found that the microglial compartment was reconstituted within 1 week of depletion. Microglia repopulation relied on CNS-resident cells, independent from bone-marrow-derived precursors. During repopulation, microglia formed clusters of highly proliferative cells that migrated apart once steady state was achieved. Proliferating microglia expressed …

Central Nervous SystemCellular differentiationCentral nervous systemInterleukin-1betaImmunologyCX3C Chemokine Receptor 1Bone Marrow CellsBiologyMiceCell MovementCX3CR1medicineAnimalsImmunology and AllergyProgenitor cellNeuroinflammationCell ProliferationReceptors Interleukin-1 Type IMicrogliaBase SequenceTumor Necrosis Factor-alphaMacrophagesCell DifferentiationSequence Analysis DNAHematopoietic Stem CellsCell biologyMice Inbred C57BLmedicine.anatomical_structureInfectious DiseasesImmunologyTumor necrosis factor alphaReceptors ChemokineMicrogliaSignal transductionSignal TransductionImmunity
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IL-23-mediated mononuclear phagocyte crosstalk protects mice from Citrobacter rodentium-induced colon immunopathology.

2014

Gut homeostasis and mucosal immune defense rely on the differential contributions of dendritic cells (DC) and macrophages. Here we show that colonic CX3CR1+ mononuclear phagocytes are critical inducers of the innate response to Citrobacter rodentium infection. Specifically, the absence of IL-23 expression in macrophages or CD11b+ DC results in the impairment of IL-22 production and in acute lethality. Highlighting immunopathology as a death cause, infected animals are rescued by the neutralization of IL-12 or IFNγ. Moreover, mice are also protected when the CD103+ CD11b− DC compartment is rendered deficient for IL-12 production. We show that IL-12 production by colonic CD103+ CD11b− DC is r…

ChemokineColonCX3C Chemokine Receptor 1General Physics and Astronomychemical and pharmacologic phenomenaMice TransgenicInterleukin-23General Biochemistry Genetics and Molecular BiologyMonocytesArticleMicrobiologyInterferon-gammaMiceIntestinal mucosaAntigens CDImmunopathologyCitrobacter rodentiummedicineAnimalsHomeostasisInterferon gammaIntestinal MucosaImmunity MucosalMultidisciplinaryCD11b AntigenbiologyInterleukinsMacrophagesEnterobacteriaceae InfectionsGeneral ChemistryMononuclear phagocyte systemDendritic CellsInterleukin-12Survival AnalysisImmunity InnateIntegrin alpha MGene Expression RegulationImmunologyInterleukin 12biology.proteinCitrobacter rodentiumTh17 CellsReceptors ChemokineIntegrin alpha Chainsmedicine.drugSignal TransductionNature communications
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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