Search results for "Lectin"

showing 10 items of 495 documents

A role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndrome.

2012

The anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonis…

LipopolysaccharidesNeutrophilsImmunology610 MedizinImmunoglobulinslcsh:MedicineInflammationApoptosisImmunopathologyBiologyNeutrophil ActivationAutoimmune DiseasesPhagocytosisimmune system diseases610 Medical sciencesmedicineHumansInterleukin 8L-SelectinReceptorlcsh:ScienceBiologyImmune ResponseneoplasmsRespiratory BurstInflammationToll-like receptorMultidisciplinaryInnate immune systemCD11b AntigenCoagulation DisordersEffectorInterleukin-8lcsh:RImmunityHematologyAntiphospholipid SyndromeFlow CytometryInnate ImmunityRespiratory burstToll-Like Receptor 4ImmunologyTLR4MedicineClinical Immunologylcsh:Qmedicine.symptomResearch ArticleSignal TransductionPLoS ONE
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Effect of Pro-inflammatory Stimuli on Tumor Cell-Mediated Induction of Endothelial Cell Adhesion Molecules in Vitro

2002

The object of our study was the question about the relevance of the tumor surrounding inflammatory cells with respect to the metastatic potential of the tumor cells. To imitate the role of inflammatory cells, three colon carcinoma (HT-29, HRT-18, and SW-620), one breast carcinoma (MCF-7), and one melanoma (ST-ML-12) cell lines were treated with pro-inflammatory stimuli, LPS, TNF-alpha, or IL-1beta. HUVEC monolayers were then stimulated by the collected supernatants (SN) of the tumor cells, following washing out of the applied stimuli. Analysis of CAM expression on HUVEC was performed using cell enzyme immunoassay. E-selectin, VCAM-1, and, in part, ICAM-1 were significantly up-regulated on H…

LipopolysaccharidesPathologymedicine.medical_specialtyEndotheliummedicine.medical_treatmentClinical BiochemistryCellVascular Cell Adhesion Molecule-1Breast NeoplasmsBiologyPathology and Forensic MedicineImmunoenzyme TechniquesNeoplasmsE-selectinTumor Cells CulturedmedicineHumansMelanomaMolecular BiologyCells CulturedInflammationTumor Necrosis Factor-alphaCell adhesion moleculeCarcinomaIntercellular Adhesion Molecule-1Up-Regulationmedicine.anatomical_structureCytokineTumor progressionCell cultureCulture Media ConditionedColonic Neoplasmsbiology.proteinCancer researchFemaleTumor necrosis factor alphaEndothelium VascularE-SelectinCell Adhesion MoleculesInterleukin-1Experimental and Molecular Pathology
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Endothelialization and Anticoagulation Potential of Surface-Modified PET Intended for Vascular Applications.

2018

In vascular tissue engineering, great attention is paid to the immobilization of biomolecules onto synthetic grafts to increase bio- and hemocompatibility-two critical milestones in the field. The surface modification field of poly(ethylene terephthalate) (PET), a well-known vascular-graft material, is matured and oversaturated. Nevertheless, most developed methods are laborious multistep procedures generally accompanied by coating instability or toxicity issues. Herein, a straightforward surface modification procedure is presented engineered to simultaneously promote surface endothelialization and anticoagulation properties via the covalent immobilization of gelatin through a photoactivate…

LipopolysaccharidesPolymers and PlasticsPoly(ethylene terephthalate)Gene ExpressionBiocompatible Materials02 engineering and technology01 natural sciencesGelatinendothelializationchemistry.chemical_compoundCoatingPolyethylene terephthalateMaterials Chemistrychemistry.chemical_classificationPolyethylene TerephthalatesSurface modifiedhemocompatibility021001 nanoscience & nanotechnologyPlatelet Endothelial Cell Adhesion Molecule-10210 nano-technologyE-Selectinbiotechnologyendotoxin contentazide photograftingAzidesfood.ingredientMaterials scienceBiocompatibilityCell SurvivalSurface PropertiesBioengineeringengineering.material010402 general chemistryBiomaterialsfoodvon Willebrand FactorHuman Umbilical Vein Endothelial CellsHumansTissue EngineeringBiomoleculeAnticoagulants0104 chemical sciencesBlood Vessel ProsthesischemistryengineeringSurface modificationBlood VesselsGelatinAzideBiomarkersBiomedical engineeringMacromolecular bioscience
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Resistance of natural killer T cell-deficient mice to systemic Shwartzman reaction.

2000

The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12-induced interferon (IFN)-gamma production at the priming stage. We examined the involvement in the priming mechanism of the unique population of Valpha14 natural killer T (NKT) cells because they promptly produce IFN-gamma after IL-12 stimulation. We report here that LPS- or IL-12-primed NKT cell genetically deficient mice were found to be resistant to LPS-elicited mortality. This outcome can be attributed to the reduction of IFN-gamma production, because injection of recombinant mouse IFN-gamma, but not injection of IL-12, effectively primed the NKT …

LipopolysaccharidesShwartzman phenomenonReceptors Antigen T-Cell alpha-betaImmunologyPopulationPriming (immunology)Mice SCIDBiologyLymphocyte DepletionInterferon-gammaMiceInterferonmedicineImmunology and AllergyAnimalsInterferon gammaLectins C-TypeAntigenseducationeducation.field_of_studyMice Inbred BALB Cinterferon γTumor Necrosis Factor-alphalipopolysaccharideBrief Definitive ReportInterleukinProteinsShwartzman reactionNatural killer T cellmedicine.diseaseInterleukin-12Immunity Innatenatural killer T cellsKiller Cells NaturalMice Inbred C57BLImmunologyAntigens SurfaceInterleukin 12interleukin 12medicine.drugNK Cell Lectin-Like Receptor Subfamily BShwartzman PhenomenonThe Journal of experimental medicine
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Ciona intestinalis galectin (CiLgals-a and CiLgals-b) genes are differentially expressed in endostyle zones and challenged by LPS

2015

Abstract Immunohistochemical and in situ hybridization assays were performed to answer the question whether the endostyle, that is the initial gastro-intestinal trait of Ciona intestinalis pharynx, is involved in galectin (CiLgals-a and CiLgals-b) production during the pharynx inflammatory response to LPS inoculation. Specific anti-CiLgal-a and anti-CiLgals-b antibodies, and oligonucleotide probes, that mark inflammatory hemocytes inside the pharynx vessels and vessel epithelium as shown by a previous paper, were assayed on endostyle histological sections. For the first time, we show that galectins are produced by endostyle zones, and both CiLgals-a and –b genes are upregulated by LPS. CiLg…

LipopolysaccharidesSignal peptideLPSAscidianGalectinsOligonucleotidesSettore BIO/05 - ZoologiaIn situ hybridizationAquatic ScienceBiologyendostyleDownregulation and upregulationotorhinolaryngologic diseasesmedicineExtracellularAnimalsEnvironmental ChemistryCiona intestinalisIn Situ HybridizationGalectinAscidian Galectin Endostyle Inflammation Ciona intestinalisgalectinGeneral Medicinebiology.organism_classificationImmunohistochemistryMolecular biologyEpitheliumCiona intestinalismedicine.anatomical_structureItalyinflammationImmunologyPharynxEndostyle
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Application of X-ray microanalysis to study of the expression of endothelial adhesion molecules on human umbilical vein endothelial cells in vitro

1994

A semi-quantitative procedure is described, which allows the evaluation of expression levels of endothelial adhesion molecules on cultured human umbilical vein endothelial cells (HUVEC) using energy dispersive X-ray microanalysis (EDX). As a model two adhesion molecules, E-selection (CD62E; ELAM-1/endothelial leukocyte adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1; CD54), were localized by the use of the silver-enhancement colloidal gold method after stimulation of HUVEC with endotoxin lipopolysaccharide (LPS), tumour necrosis factor (TNF) or a phorbol ester (PMA). The analysis was performed in a scanning electron microscope (SEM) at an accelerating voltage of 15 kV wit…

LipopolysaccharidesUmbilical VeinsHistologyEndotheliumEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesUmbilical veinE-selectinmedicineHumansMolecular BiologyCells CulturedbiologyTumor Necrosis Factor-alphaChemistryCell adhesion moleculeCell BiologyGeneral MedicineImmunogold labellingAdhesionIntercellular Adhesion Molecule-1ImmunohistochemistryMolecular biologyStimulation ChemicalIn vitroMedical Laboratory Technologymedicine.anatomical_structurebiology.proteinTetradecanoylphorbol AcetateTumor necrosis factor alphaEndothelium VascularAnatomyE-SelectinGeneral Agricultural and Biological SciencesCell Adhesion MoleculesElectron Probe MicroanalysisHistochemistry
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IL-10 down-regulates T cell activation by antigen-presenting liver sinusoidal endothelial cells through decreased antigen uptake via the mannose rece…

1998

SUMMARYOur study demonstrates that antigen-presenting liver sinusoidal endothelial cells (LSEC) induce production of interferon-gamma (IFN-γ) from cloned Th1 CD4+ T cells. We show that LSEC used the mannose receptor for antigen uptake, which further strengthened the role of LSEC as antigen-presenting cell (APC) population in the liver. The ability of LSEC to activate cloned CD4+ T cells antigen-specifically was down-regulated by exogenous prostaglandin E2 (PGE2) and by IL-10. We identify two separate mechanisms by which IL-10 down-regulated T cell activation through LSEC. IL-10 decreased the constitutive surface expression of MHC class II as well as of the accessory molecules CD80 and CD86 …

Liver cytologyT cellT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsDown-RegulationReceptors Cell SurfaceBiologyLymphocyte ActivationDinoprostoneMiceAntigenAntigens CDmedicineImmunology and AllergyAnimalsLectins C-TypeCD86Antigen PresentationMice Inbred BALB CMembrane GlycoproteinsHistocompatibility Antigens Class IIOriginal ArticlesInterleukin-10Interleukin 10medicine.anatomical_structureMannose-Binding LectinsLiverImmunologyB7-1 AntigenCytokinesFemaleB7-2 AntigenEndothelium VascularMannoseCD80Mannose receptorMannose ReceptorClinical and experimental immunology
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Involvement of complement pathways in patients with bacterial septicemia.

2007

The complement system is a major humoral portion of the innate immune system, playing a significant role in host defence against microorganisms. The biological importance of this system is underlined by the fact that at least three different pathways for its activation exist, the classical, the MBL and the alternative pathway. To elucidate the involvement of the classical and/or the MBL pathway during bacterial septicemia, 32 patients with gram-positive and 30 patients with gram-negative bacterial infections were investigated. In patients with gram-positive bacteria, a significant consumption of C1q (p=0.005) but not of mannose-binding lectin (MBL) (p=0.2) was found during the acute phase o…

MESH: Complement Pathway Mannose-Binding LectinLipopolysaccharidesSalmonellaMESH: Complement C1qLipopolysaccharideImmunologychemical and pharmacologic phenomenaBacteremiamedicine.disease_causeGram-Positive BacteriaMannose-Binding LectinMicrobiologyMESH: Gram-Positive Bacteria03 medical and health scienceschemistry.chemical_compoundClassical complement pathway0302 clinical medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyComplement Pathway ClassicalMESH: BacteremiaMolecular Biology030304 developmental biology0303 health sciencesInnate immune systemMESH: HumansbiologyComplement C1qLectinSalmonella entericaComplement Pathway Mannose-Binding LectinMESH: Complement Pathway Classicalbiology.organism_classificationbacterial infections and mycoses3. Good healthComplement systemMESH: Mannose-Binding LectinchemistryMESH: Salmonella entericaImmunologyAlternative complement pathwaybiology.proteinMESH: LipopolysaccharidesBacteria030215 immunologyMolecular immunology
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Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation

2018

Capucha et al. demonstrate that mucosal Langerhans cell (LC) differentiation from pre–dendritic cells and monocytes involves consecutive BMP7 and TGF-β1 signaling in separate anatomical locations. Moreover, mucosal microbiota regulates the development of LCs that in turn shape microbial and immunological homeostasis.

Male0301 basic medicineLangerhans cellBone Morphogenetic Protein 7ImmunologyReceptor Transforming Growth Factor-beta Type IBiologyArticle311Transforming Growth Factor beta1Mice03 medical and health sciencesDownregulation and upregulation319Langerhans cell differentiationmedicineAnimalsHumansImmunology and AllergyLectins C-TypeImmunity MucosalResearch ArticlesBone Morphogenetic Protein Receptors Type IMice KnockoutLamina propriaintegumentary systemMicrobiotaStem CellsMouth MucosaMucous membraneCell DifferentiationEpitheliumUp-RegulationCell biologyMice Inbred C57BLBone morphogenetic protein 7Mannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureLangerhans CellsAntigens SurfaceSignal transductionTranscriptomeSignal TransductionJournal of Experimental Medicine
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