Search results for "Immunity"

showing 10 items of 1537 documents

The Serine/Threonine Protein Phosphatase 2A (PP2A) Regulates Syk Activity in Human Platelets

2020

Distinct membrane receptors activate platelets by Src-family-kinase (SFK)-, immunoreceptor-tyrosine-based-activation-motif (ITAM)-dependent stimulation of spleen tyrosine kinase (Syk). Recently, we reported that platelet activation via glycoprotein (GP) VI or GPIb&alpha

Blood Platelets0301 basic medicinePlatelet AggregationPhosphataseSykchemical and pharmacologic phenomena030204 cardiovascular system & hematologyenvironment and public healthspleen tyrosine kinase (Syk)ArticleCatalysisInorganic ChemistryDephosphorylationglycoprotein VIglycoprotein Ibα03 medical and health sciences0302 clinical medicineHumansSyk KinaseProtein Phosphatase 2Platelet activationPhosphorylationPhysical and Theoretical ChemistryMolecular BiologySpectroscopyProtein kinase CChemistryKinaseprotein phosphatase 2AOrganic Chemistryhemic and immune systemsGeneral MedicineProtein phosphatase 2Protein-Tyrosine KinasesPlatelet Activation3. Good healthComputer Science ApplicationsCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologyplateletsPhosphorylationbiological phenomena cell phenomena and immunitySignal TransductionInternational Journal of Molecular Sciences
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Platelet, Not Endothelial, P-Selectin Expression Contributes to Generation of Immunity in Cutaneous Contact Hypersensitivity

2010

Leukocyte extravasation is a prerequisite for host defense and autoimmunity alike. Detailed understanding of the tightly controlled and overlapping sequences of leukocyte extravasation might aid development of novel therapeutic strategies. Leukocyte extravasation is initiated by interaction of selectins with appropriate carbohydrate ligands. Lack of P-selectin expression leads to decreased contact hypersensitivity responses. Yet, it remains unclear if this is due to inhibition of leukocyte extravasation to the skin or due to interference with initial immune activation in lymph nodes. In line with previous data, we here report a decreased contact hypersensitivity response, induced by 2,4,-di…

Blood PlateletsAdoptive cell transferP-selectinInflammationDermatitis ContactPathology and Forensic MedicineMiceImmunityMedicineAnimalsBlood Platelets/*metabolismCell ShapeSkinInflammationbusiness.industryImmunityEndothelial CellsSkin/immunology/*pathologyDermatitis Contact/complications/*immunology/*pathologyLeukocyte extravasationAdoptive TransferInflammation/complications/immunology/pathologyEndothelial stem cellMice Inbred C57BLP-Selectinmedicine.anatomical_structureImmunologyEndothelial Cells/*metabolismDinitrofluorobenzeneBone marrowmedicine.symptomImmunity/*immunologybusinessSelectinP-Selectin/*metabolismRegular Articles
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TREM-1 ligand expression on platelets enhances neutrophil activation

2007

Abstract The triggering receptor expressed on myeloid cells 1 (TREM-1) plays an important role in the innate immune response related to severe infections and sepsis. Modulation of TREM-1–associated activation improves the outcome in rodent models for pneumonia and sepsis. However, the identity and occurrence of the natural TREM-1 ligands are so far unknown, impairing the further understanding of the biology of this receptor. Here, we report the presence of a ligand for TREM-1 on human platelets. Using a recombinant TREM-1 fusion protein, we demonstrate specific binding of TREM-1 to platelets. TREM-1–specific signals are required for the platelet-induced augmentation of polymorphonuclear leu…

Blood PlateletsLipopolysaccharidesIntegrinsNeutrophilsRecombinant Fusion ProteinsImmunologyIntegrinLigandsBiochemistryNeutrophil ActivationSepsisMiceImmunitySepsismedicineAnimalsHumansPlateletReceptors ImmunologicReceptorMembrane GlycoproteinsInnate immune systembiologyPneumoniaCell BiologyHematologymedicine.diseaseFusion proteinImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Disease Models AnimalGene Expression RegulationImmunologySelectinsbiology.proteinSelectinProtein BindingBlood
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Pertussis-specific cell-mediated immunity in infants after vaccination with a tricomponent acellular pertussis vaccine.

1996

The aim of this study was to investigate pertussis-specific cell-mediated immunity in infants vaccinated with a tricomponent acellular vaccine. Infants were investigated during a primary vaccination schedule from the third month of life to the sixth month as well as before and after a booster at 15 to 24 months. This is the first report of specific cell-mediated immune responses to pertussis-related antigens in infants below the age of 12 months. Our data show that the vaccine induces T-cell responses specific for the vaccine components, detoxified pertussis toxin, filamentous hemagglutinin, and pertactin, that increase progressively over the course of the vaccination schedule. In contrast …

Bordetella pertussisCellular immunityVaccination scheduleT-LymphocytesImmunologyLymphocyte ActivationMicrobiologyBordetella pertussisImmunophenotypingImmune systemImmunityHumansVirulence Factors BordetellaAntigens BacterialbiologyVaccinationInfantbiology.organism_classificationVirologyAntibodies BacterialVaccinationInfectious DiseasesPertussis ToxinImmunologyCytokinesParasitologyCytokine secretionPertactinResearch Article
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Acute Laryngitis in the Rat Induced by Moraxella catarrhalis and Bordetella pertussis: Number of Neutrophils, Dendritic Cells, and T and B Lymphocyte…

1999

Infectious laryngotracheitis results in fulminant respiratory distress. During the disease, the subglottic mucosa is selectively infected and swollen, the reason for this preference being unknown. Therefore, in the present study the immunoreaction of the laryngeal mucosa was studied in the rat after inhalation of either heat-killed Moraxella catarrhalis (PVG rats) or application of viable Bordetella pertussis (BN rats). The number of neutrophils, macrophages, dendritic cells, and T and B lymphocytes was determined in the mucosa of the supraglottic, glottic, and subglottic area of the larynx as well as in the trachea. After application of the pathogens, the mucosa of the subglottic area was …

Bordetella pertussisPathologymedicine.medical_specialtyNeutrophilsWhooping CoughNeisseriaceae InfectionsT-LymphocytesInflammationGranulocyteBordetella pertussisMoraxella catarrhalisLaryngitismedicineAnimalsImmunity MucosalB-Lymphocytesbiologybusiness.industryRespiratory diseaseDendritic CellsT lymphocyteDendritic cellbiology.organism_classificationmedicine.diseaseEpitheliumBlood Cell CountRatsmedicine.anatomical_structureLaryngeal MucosaOrgan SpecificityPediatrics Perinatology and Child HealthImmunologymedicine.symptombusinessMoraxella catarrhalisPediatric Research
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Analogous IgG subclass response to pertussis toxin in vaccinated children, healthy or affected by whooping cough

2003

The study of antigen specific IgG subclass distribution during disease, or during any other natural or artificial immunisation, can provide useful information on the kind of the immune response and the expected levels of protection. This is particularly true for diseases, such as pertussis in which the mechanisms underlying specific defence are still not completely understood. An investigation was therefore performed to evaluate the IgG subclass response to pertussis toxin (PT) in sera from 89 healthy vaccinated children and 131 vaccinated or unvaccinated children convalescent after a confirmed B. pertussis symptomatic infection. Antibody titres were expressed in arbitrary ELISA units/ml, a…

Bordetella pertussisWhooping CoughEnzyme-Linked Immunosorbent AssayPertussis toxinBordetella pertussisSubclassImmune systemReference ValuesmedicineHumansChildWhooping coughPertussis VaccineGeneral VeterinaryGeneral Immunology and MicrobiologybiologyPublic Health Environmental and Occupational Healthmedicine.diseasebiology.organism_classificationAntibodies BacterialVirologyVaccinationInfectious DiseasesPertussis ToxinImmunoglobulin GHumoral immunityImmunologybiology.proteinMolecular MedicineAntibodyVaccine
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Characterization of grapevine defense reactions and identification of elicitors : the endopolygalacturonase 1 from Botrytis cinerea, an avirulence fu…

2002

The fight against grapevine pathogens is mainly carried out by pesticides, the continued use of which is harmful to the environment and the health of users and consumers. The main organizations in charge of viticulture set as a priority the research and use of alternatives to chemical control. However, the genetic improvement of the vine is prohibited in AOC vineyards to preserve the varietal typicity, partly responsible for the quality of the wines. In addition, research undertaken some fifteen years ago reveals that plants have their own immune defenses, which they activate on contact with the microorganisms they recognize via molecules called elicitors. In this context, the objective of …

Botrytis cinerea endopolygalacturonase 1signalisation cellulaireBotrytis cinerea.[SDV.EE.IEO] Life Sciences [q-bio]/Ecology environment/Symbiosisprotectionoligogalacturonatesavirulencelaminarinegrapevinevirulenceréactions de défenseelicitorsVitis viniferadefense reactionséliciteurs[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biologycell signalingoligogalacturonidesendopolygalacturonase 1 de Botrytis cinereavigne[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunitylaminarin[SDV.BV.PEP] Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacy
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Cigarette smoke alters IL-33 expression and release in airway epithelial cells

2014

AbstractAirway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show red…

Bronchial epithelial cellLipopolysaccharidesBlotting WesternBronchiInflammationRespiratory MucosaBiologyReal-Time Polymerase Chain ReactionBronchoalveolar LavageImmunoenzyme TechniquesBronchial epithelial cell; COPD; Cigarette smoke; IL-33; InflammationSmokeacute lung injury cigarette smokeinterleukin 33medicineCOPDHumansRNA MessengerReceptorMolecular BiologyCells CulturedCell ProliferationInflammationToll-like receptorInnate immune systemReverse Transcriptase Polymerase Chain ReactionInterleukinsCigarette smokeFlow CytometryInterleukin-33Immunity Innaterespiratory tract diseasesCell biologyToll-Like Receptor 4Interleukin 33ImmunologyIL-33TLR4Molecular MedicineRespiratory epitheliummedicine.symptomIntracellularBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Th17 immunity in children with allergic asthma and rhinitis: a pharmacological approach

2013

Th17 cells and IL-17A play a role in the development and progression of allergic diseases. We analyzed the IL-17A levels in sputum supernatants (Ss), nasal wash (NW) and plasma (P) from Healthy Controls (HC) and children with Asthma/Rhinitis. We tested the expression of IL-17A, RORγ(t) and FOXP3 in peripheral blood T-lymphocytes from intermittent and mild-moderate asthma. The effect of Budesonide and Formoterol was tested "in vitro" on IL-17A, RORγ(t) and FOXP3 expression in cultured T-lymphocytes from mild-moderate asthma/persistent rhinitis patients, and on nasal and bronchial epithelial cells stimulated with NW and Ss from mild-moderate asthma/persistent rhinitis. Further, the effect of …

BudesonideMalePulmonologyIL 13 and AsthmaGene ExpressionAnti-asthmatic AgentBiochemistryPediatricsimmune system diseasesFormoterol FumarateMolecular Cell BiologyAnti-Asthmatic AgentsBudesonideChildCells CulturedMultidisciplinaryImmune System ProteinsQInterleukin-17RFOXP3Forkhead Transcription FactorsNuclear Receptor Subfamily 1 Group F Member 3EthanolaminesMedicineFemaleInterleukin 17medicine.symptommedicine.drugResearch ArticleRhinitis Allergic PerennialAdolescentScienceImmunologyPediatric PulmonologyInflammationAdministration InhalationmedicineHumansAdrenergic beta-2 Receptor AgonistsBiologyAsthmaInflammationbusiness.industryInterleukin-8SputumImmunityProteinsImmunologic Subspecialtiesmedicine.diseaseNasal Lavage FluidAsthmarespiratory tract diseasesCase-Control StudiesImmunologySputumTh17 CellsClinical ImmunologyFormoterolbusinessPulmonary Immunology
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CTCF and BORIS Regulate Rb2/p130 Gene Transcription: A Novel Mechanism and a New Paradigm for Understanding the Biology of Lung Cancer

2011

Abstract Although innumerable investigations regarding the biology of lung cancer have been carried out, many aspects thereof remain to be addressed, including the role played by the retinoblastoma-related protein Rb2/p130 during the evolution of this disease. Here we report novel findings on the mechanisms that control Rb2/p130 gene expression in lung fibroblasts and characterize the effects of Rb2/p130 deregulation on the proliferative features of lung cancer cells. We revealed for the first time that in lung fibroblasts the expression of Rb2/p130 gene is directly controlled by the chromatin insulator CCCTC-binding factor, CTCF, which by binding to the Rb2/p130 gene promoter induces, and/…

CCCTC-Binding FactorChromatin ImmunoprecipitationCancer ResearchLung NeoplasmsTranscription GeneticSettore MED/06 - Oncologia MedicaBiologyInsulator (genetics)Open Reading FramesTranscription (biology)Carcinoma Non-Small-Cell LungCell Line TumorGene expressionmedicineHumansCarcinoma Small CellPromoter Regions GeneticLung cancerChromosome PositioningMolecular BiologyGeneBinding SitesRetinoblastoma-Like Protein p130PromoterFibroblastsmedicine.diseaseChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsGene transcriptionOncologyCTCFembryonic structuresCancer researchLung cancerLung cancer; Gene transcriptionbiological phenomena cell phenomena and immunityProtein BindingMolecular Cancer Research
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