Search results for " CCR2"

showing 6 items of 6 documents

Intervention of Inflammatory Monocyte Activity Limits Dermal Fibrosis

2019

Monocytes and monocyte-derived cells are important players in the initiation, progression, and resolution of inflammatory skin reactions. As inflammation is a prerequisite for fibrosis development, we focused on the role of monocytes in cutaneous fibrosis, the clinical hallmark of patients suffering from systemic sclerosis. Investigating the function of monocytes in reactive oxygen species–induced dermal fibrosis, we observed that early monocyte depletion partially reduced disease severity. Low numbers of inflammatory Ly6Chigh monocytes, as well as inhibition of CCR2 and CCL2 in wild type animals by a specific L-RNA aptamer, mitigated disease parameters, indicating a pivotal role for CCR2+ …

0301 basic medicineCCR2Nerve growth factor IBReceptors CCR2InflammationDermatologyCCL2BiochemistryMonocytesSclerodermaMiceRandom Allocation03 medical and health sciences0302 clinical medicineReference ValuesFibrosisNuclear Receptor Subfamily 4 Group A Member 1medicineAnimalsHumansMolecular BiologyCells CulturedChemokine CCL2InflammationScleroderma Systemicbusiness.industryMonocyteInterferon-stimulated geneBiopsy NeedleCell Biologymedicine.diseaseImmunohistochemistryMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisImmunologymedicine.symptombusinessSignal TransductionJournal of Investigative Dermatology
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NFATc1 releases BCL6-dependent repression of CCR2 agonist expression in peritoneal macrophages fromSaccharomyces cerevisiaeinfected mice

2016

The link between the extensive usage of calcineurin (CN) inhibitors cyclosporin A and tacrolimus (FK506) in transplantation medicine and the increasing rate of opportunistic infections within this segment of patients is alarming. Currently, how peritoneal infections are favored by these drugs, which impair the activity of several signaling pathways including the Ca(++) /CN/NFAT, Ca(++) /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is unknown. Here, we show that Saccharomyces cerevisiae infection of peritoneal resident macrophages triggers the transient nuclear translocation of NFATc1β isoforms, resulting in a coordinated, CN-dependent induction of the Ccl2, Ccl7, and Ccl12 genes, all enc…

0301 basic medicineChemokineReceptors CCR2Calcineurin InhibitorsImmunologySaccharomyces cerevisiaeOpportunistic InfectionsCCL7MonocytesMice03 medical and health sciences0302 clinical medicineCyclosporin aAnimalsProtein IsoformsImmunology and AllergyChemokine CCL7Promoter Regions GeneticCCL12Transcription factorChemokine CCL2NFATC Transcription FactorsbiologyCalcineurinNF-kappa BNFATNFATC Transcription FactorsMonocyte Chemoattractant Proteins3. Good healthCalcineurinProtein Transport030104 developmental biology030220 oncology & carcinogenesisMacrophages PeritonealProto-Oncogene Proteins c-bcl-6biology.proteinCancer researchEuropean Journal of Immunology
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The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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CD73 Overexpression in Podocytes: A Novel Marker of Podocyte Injury in Human Kidney Disease

2021

The CD73 pathway is an important anti-inflammatory mechanism in various disease settings. Observations in mouse models suggested that CD73 might have a protective role in kidney damage

Male0301 basic medicinePathologyCCR2podocyte030232 urology & nephrologyGene ExpressionKidneyPodocyte0302 clinical medicineFocal segmental glomerulosclerosisMedicineMinimal change diseaseBiology (General)5'-NucleotidaseSpectroscopyAged 80 and overKidneymedicine.diagnostic_testPodocytesGlomerulonephritisGeneral MedicineMiddle AgedComputer Science ApplicationsChemistryProteinuriaminimal change diseasemedicine.anatomical_structureImmunohistochemistryFemaleKidney DiseasesAdultmedicine.medical_specialtyQH301-705.5Receptors CCR2GPI-Linked ProteinsImmunofluorescenceArticleCatalysisInorganic Chemistry03 medical and health sciencesHumansPhysical and Theoretical ChemistryQD1-999Molecular BiologyAgedbusiness.industryOrganic Chemistrymedicine.disease030104 developmental biologyGene Expression RegulationCD73CCR2businessBiomarkersInternational Journal of Molecular Sciences
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Enhanced glomerular Toll-like receptor 4 expression and signaling in patients with type 2 diabetic nephropathy and microalbuminuria

2014

Toll-like receptor 4 (TLR4), a component of the innate immune system, is recognized to promote tubulointerstitial inflammation in overt diabetic nephropathy (DN). However, there is no information on immune activation in resident renal cells at an early stage of human DN. In order to investigate this, we studied TLR4 gene and protein expression and TLR4 downward signaling in kidney biopsies of 12 patients with type 2 diabetes and microalbuminuria, and compared them with 11 patients with overt DN, 10 with minimal change disease (MCD), and control kidneys from 13 patients undergoing surgery for a small renal mass. Both in microalbuminuria and in overt DN, TLR4 mRNA and protein were overexpress…

MaleKidney GlomerulusDiabetic nephropathyurologic and male genital diseasesDiabetic nephropathynefropatiadiabeticaDiabetic NephropathiesMinimal change diseaseChemokine CCL5KidneyMiddle AgedUp-RegulationKidney Tubulesmedicine.anatomical_structureNephrologyDisease ProgressionFemaleHumanSignal Transductionmedicine.medical_specialtyReceptors CCR5Receptors CCR2NephrosisAntigens Differentiation MyelomonocyticFollow-Up StudieNephropathyToll-like receptorAntigens CDDiabetes mellitusInternal medicinemedicineAlbuminuriaHumansRNA MessengerInflammationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryNephrosis LipoidKidney TubuleTranscription Factor RelABiomarkermedicine.diseaseImmunity InnateToll-Like Receptor 4EndocrinologyDiabetes Mellitus Type 2Diabetic NephropathieTLR4MicroalbuminuriaKidney GlomerulubusinessBiomarkersMicroalbuminuriaFollow-Up StudiesKidney International
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Second-generation Langerhans cells originating from epidermal precursors are essential for CD8+ T cell priming.

2014

Abstract In vivo studies questioned the ability of Langerhans cells (LCs) to mediate CD8+ T cell priming. To address this issue, we used intradermal immunization with plasmid DNA, a system in which activation of CD8+ T cells depends on delayed kinetics of Ag presentation. We found that dendritic cells (DCs) located in the skin at the time of immunization have limited ability to activate CD8+ T cells. This activity was mediated by a second generation of DCs that differentiated in the skin several days after immunization, as well as by lymph node–resident DCs. Intriguingly, CD8+ T cell responses were not affected following treatment with clodronate liposomes, immunization of CCR2−/− mice, or …

Receptors CCR2T cellImmunologyPriming (immunology)CD11cchemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMiceImmune systemGiant Cells LanghansmedicineImmunology and AllergyCytotoxic T cellAnimalsSkinMice KnockoutChemokine CCL20integumentary systemhemic and immune systemsCell DifferentiationDendritic CellsMolecular biologyCD11c AntigenCCL20Mice Inbred C57BLmedicine.anatomical_structureImmunologyIntercellular Signaling Peptides and ProteinsClodronic AcidCD8Ex vivoHeparin-binding EGF-like Growth FactorPlasmidsJournal of immunology (Baltimore, Md. : 1950)
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