Search results for "SENSITIZATION"

showing 10 items of 237 documents

Insect venom immunotherapy induces interleukin-10 production and a Th2-to-Th1 shift, and changes surface marker expression in venom-allergic subjects.

1997

Abstract The current study was carried out to elucidate the immunoregulatory changes induced by venom immunotherapy (VIT) in bee or wasp allergic subjects. All subjects included in this study had a history of severe systemic allergic reactions to stings of the respective insect as well as positive skin tests with the respective venom or venom-specific IgE in the sera. Parameters assessed in peripheral blood mononuclear cells (PBMC) before and after initiation of VIT (rush therapy reaching a maintenance dose of 100 micrograms venom injected subcutaneously within 1 week) were expression of CD3, CD4, CD8, CD45RA, CD45RO, interleukin (IL)-2 receptor (R) alpha, IL-4R, IL-12R, Fc epsilon RII, CD4…

Time Factorsmedicine.medical_treatmentImmunologyCD40 LigandDown-RegulationVenomWasp VenomsImmunoglobulin ELigandsLymphocyte ActivationPeripheral blood mononuclear cellInterferon-gammaTh2 CellsAntigens CDT-Lymphocyte SubsetsmedicineImmunology and AllergyHumansLymphocyte CountRNA MessengerCD40 AntigensCD40Membrane GlycoproteinsbiologyReceptors IgEInterleukinAntibodies MonoclonalInsect Bites and StingsReceptors InterleukinAllergensTh1 CellsInterleukin-10Receptors Interleukin-4Interleukin 10Bee VenomsCytokineDesensitization ImmunologicImmunologyAntigens Surfacebiology.proteinInterleukin-4AntibodyEuropean journal of immunology
researchProduct

Exposure to Toll like Receptor 7 (TLR7)-Ligand Supports Sensitization to an Inhaled Allergen.

2009

Toll-like receptorAllergenmedicine.anatomical_structureChemistryImmunologymedicineTLR7medicine.disease_causeLigand (biochemistry)SensitizationB102. IMMUNE MECHANISMS IN THE AIRWAY AND RESPONSE TO INJURY AND INFECTION
researchProduct

Regulatory T Cells More Effectively Suppress Th1-Induced Airway Inflammation Compared with Th2

2011

Abstract Asthma is a syndrome with different inflammatory phenotypes. Animal models have shown that, after sensitization and allergen challenge, Th2 and Th1 cells contribute to the development of allergic airway disease. We have previously demonstrated that naturally occurring regulatory T cells (nTregs) can only marginally suppress Th2-induced airway inflammation and airway hyperresponsiveness. In this study, we investigated nTreg-mediated suppression of Th2-induced and Th1-induced acute allergic airway disease. We demonstrate in vivo that nTregs exert their suppressive potency via cAMP transfer on Th2- and Th1-induced airway disease. A comparison of both phenotypes revealed that, despite …

TransgeneImmunologyMice TransgenicInflammationT-Lymphocytes RegulatoryMiceTh2 CellsIn vivoImmunitymedicineAnimalsImmunology and AllergyPotencyCells CulturedSensitizationAsthmaInflammationMice KnockoutMice Inbred BALB Cbusiness.industryTh1 Cellsrespiratory systemmedicine.diseasePhenotypeCoculture TechniquesImmunity Innaterespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureAcute DiseaseImmunologyFemaleDisease SusceptibilityBronchial Hyperreactivitymedicine.symptombusinessThe Journal of Immunology
researchProduct

Efficiency of Biolistic DNA Vaccination in Experimental Type I Allergy

2012

Gene gun-mediated delivery of allergen-encoding plasmid DNA has been in focus for many years now as being a needle-free alternative to the protein-based desensitization regimen used in specific immunotherapy. Biolistic immunization with the Helios gene gun has proven to be potent in the induction of antigen-specific CD4(+) and CD8(+) T cells. Here we describe biolistic vaccination in experimental mouse models of IgE-mediated type I allergy as well as allergen-induced airway inflammation.

Vaccinationbusiness.industrymedicine.medical_treatmentImmunologyAirway inflammationType i allergyMedicinebusinessGeneCD8Gene gunDNA vaccinationDesensitization (medicine)
researchProduct

Agonist and antagonist-dependent internalization of the human vasopressin V2 receptor.

1998

Abstract In this report we demonstrate that in HEK293 cells stably expressing the human V2vasopressin receptor, ligand-induced internalization of the hormone receptor occurs via the clathrin-dependent pathway. Studies of receptor trafficking either by direct visualization of the V2receptor by confocal microscopy or binding experiments show a rapid internalization (half-time 6–7 min). Blocking of the clathrin-dependent pathway by hypertonic sucrose increased vasopressin-induced cellular cAMP production and decreased the desensitization of the V2receptor–adenylyl cyclase system. Thus, internalization appears to be a major regulatory mechanism terminating vasopressin action in HEK293 cells. Tw…

VasopressinReceptors VasopressinTime Factorsmedia_common.quotation_subjectRecombinant Fusion ProteinseducationBiologyKidneyLigandsTransfectionlaw.inventionCell LineEpitopesDesensitization (telecommunications)Confocal microscopylawEnzyme-linked receptorHumansInternalizationReceptormedia_commonAntagonistCell BiologyClathrinPeptide FragmentsCell biologyHormone receptorAntidiuretic Hormone Receptor AntagonistsExperimental cell research
researchProduct

Viral Components Enhance Antigen Presentation And Induce Sensitization Towards Harmless Inhaled Antigens

2010

Viral Componentsmedicine.anatomical_structureAntigenbusiness.industryImmunologyAntigen presentationMedicinebusinessSensitizationD33. AIRWAY INFECTION: MICROBIOME AND MECHANISMS
researchProduct

Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
researchProduct

Sulfur Dioxide Oxidation Catalyzed by Photosensitized Ytterbium Diphthalocyanine

2008

Oxidation of SO2 into SO3 was found effectively catalyzed by photosensitized ytterbium diphthalocyanine, YbPc2 (Pc = phthalocyanine ligand, C32H16N8) when performed in air-saturated dimethylformamide (DMF) solution at 20 °C. The process follows according to a multi-step complex mechanism involving chemical induction as its driving force. Excitation energy of the sandwich molecular system in YbPc2 is used to promote the reaction by creating a reactive intermediate form of the ytterbium complex hosting up to eight SO2 molecules. The conversion of SO2 proved complete.

YtterbiumUV–Vis spectroscopyChemistryReactive intermediateExcited stateschemistry.chemical_elementHomogeneous catalysisGeneral ChemistryPhotochemistryHomogeneous catalysisCatalysisCatalysischemistry.chemical_compoundSulfur dioxidePhthalocyanineDimethylformamideMoleculeYtterbium diphthalocyaninePhotosensitizationOrganometallic chemistryCatalysis Letters
researchProduct

The effect of allergen immunotherapy in the onset of new sensitizations: a meta-analysis.

2017

Background Although the preventive efficacy of allergen immunotherapy (AIT) in the onset of new allergen sensitizations has been asserted by many reviews, position papers, and consensus conferences, the evidence available is from only 3 studies. The objective of this work was a systematic review to evaluate the preventive efficacy of AIT in the onset of new allergen sensitizations. The end-point was the risk difference (RD) in the onset of new allergen sensitizations between patients treated with AIT and pharmacotherapy. Methods Computerized bibliographic searches of MEDLINE, EMBASE, and the Cochrane Library (until November 30th, 2016) were done. Random-effects and fixed-effects model meta-…

allergic rhinitisPyroglyphidaenew allergen sensitizationasthmameta-analysiDesensitization ImmunologicAnti-Allergic Agentsallergen immunotherapyHypersensitivityAnimalsHumansImmunizationAntigens DermatophagoidesChildRandomized Controlled Trials as TopicInternational forum of allergyrhinology
researchProduct

Paving the way of systems biology and precision medicine in allergic diseases: the MeDALL success story: Mechanisms of the Development of ALLergy; EU…

2016

MeDALL (Mechanisms of the Development of ALLergy; EU FP7-CP-IP; Project No: 261357; 2010-2015) has proposed an innovative approach to develop early indicators for the prediction, diagnosis, prevention and targets for therapy. MeDALL has linked epidemiological, clinical and basic research using a stepwise, large-scale and integrative approach: MeDALL data of precisely phenotyped children followed in 14 birth cohorts spread across Europe were combined with systems biology (omics, IgE measurement using microarrays) and environmental data. Multimorbidity in the same child is more common than expected by chance alone, suggesting that these diseases share causal mechanisms irrespective of IgE sen…

asthma; IgE; multimorbidity; polysensitization; rhinitis.
researchProduct