0000000001118396

AUTHOR

Norbert Hilf

showing 4 related works from this author

Dendritic cell aggresome-like-induced structure formation and delayed antigen presentation coincide in influenza virus-infected dendritic cells.

2005

Abstract Influenza virus infection induces maturation of murine dendritic cells (DCs), which is most important for the initiation of an immune response. However, in contrast to EL-4 and MC57 cells, DCs present viral CTL epitopes with a delay of up to 10 h. This delay in Ag presentation coincides with the up-regulation of MHC class I molecules as well as costimulatory molecules on the cell surface and the accumulation of newly synthesized ubiquitinated proteins in large cytosolic structures, called DC aggresome-like-induced structures (DALIS). These structures were observed previously after LPS-induced maturation of DCs, and it was speculated that they play a role in the regulation of MHC cl…

Time FactorsImmunologyAntigen presentationCellAntigen-Presenting CellsEpitopes T-Lymphocytechemical and pharmacologic phenomenaBone Marrow CellsVirusCell LineMiceImmune systemCell Line TumorMHC class ImedicineImmunology and AllergyAnimalsHumansReceptors ImmunologicCells CulturedAntigen PresentationMice Inbred C3HbiologyUbiquitinViral Core ProteinsRNA-Binding ProteinsCell DifferentiationDendritic cellDendritic CellsNucleocapsid ProteinsVirologyToll-Like Receptor 2Cell biologyNucleoproteinMice Inbred C57BLToll-Like Receptor 4Aggresomemedicine.anatomical_structureNucleoproteinsInfluenza A virusbiology.proteinCytoplasmic StructuresT-Lymphocytes CytotoxicJournal of immunology (Baltimore, Md. : 1950)
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Sorafenib, but not sunitinib, affects function of dendritic cells and induction of primary immune responses

2008

AbstractThe tyrosine kinase inhibitors sorafenib and sunitinib are approved for the treatment of patients with malignant diseases. To analyze the possible use of these compounds in combination with immunotherapeutic approaches, we analyzed the effects of both inhibitors on the immunostimulatory capacity of human dendritic cells (DCs) and the induction of primary immune responses in vivo. Sorafenib, but not sunitinib, inhibits function of DCs, characterized by reduced secretion of cytokines and expression of CD1a, major histocompatibility complex, and costimulatory molecules in response to TLR ligands as well as by their impaired ability to migrate and stimulate T-cell responses. These inhib…

NiacinamideSorafenibIndolesPyridinesImmunologyAntineoplastic AgentsApoptosisCD8-Positive T-LymphocytesPharmacologyBiologyurologic and male genital diseasesMajor histocompatibility complexT-Lymphocytes RegulatoryBiochemistryPeripheral blood mononuclear cellMiceImmune systemCell MovementIn vivoSunitinibmedicineAnimalsHumansCytotoxic T cellPyrrolesCells CulturedSunitinibPhenylurea CompoundsBenzenesulfonatesGranulocyte-Macrophage Colony-Stimulating FactorDextransDendritic CellsCell BiologyHematologySorafenibEndocytosisfemale genital diseases and pregnancy complicationsMice Inbred C57BLToll-Like Receptor 4biology.proteinCytokinesFemaleInterleukin-4Lymphocyte Culture Test MixedTyrosine kinaseCell DivisionSignal Transductionmedicine.drugBlood
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Glycoprotein 96-activated dendritic cells induce a CD8-biased T cell response.

2005

Heat shock proteins (Hsps) are able to induce protective immune responses against pathogens and tumors after injection into immunocompetent hosts. The activation of components of the adaptive immune system, including cytotoxic T lymphocytes specific for pathogen- or tumor-derived peptides, is crucial for the establishment of immuno- protection. Hsps acquire these peptides during intracellular protein degradation and when released during necrotic cell death, facilitate their uptake and Minor Histocompatibility Complex (MHC)-restricted representation by professional antigen-presenting cells (APCs). In addition, the interaction of Hsps with APCs, including the Endoplasmatic Reticulum (ER)-resi…

CD4-Positive T-LymphocytesLipopolysaccharidesAntigen-Presenting CellsBone Marrow CellsMice TransgenicReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexLymphocyte ActivationBiochemistryMiceImmune systemHeat shock proteinCytotoxic T cellAnimalsHumansAntigen-presenting cellCells CulturedMembrane GlycoproteinsToll-Like ReceptorsCell DifferentiationCell BiologyDendritic cellDendritic CellsOriginal ArticlesAcquired immune systemLymphocyte SubsetsCell biologyMice Inbred C57BLToll-Like Receptor 4biology.proteinInflammation MediatorsCD8Signal TransductionCell stresschaperones
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Interaction of TLR2 and TLR4 ligands with the N-terminal domain of Gp96 amplifies innate and adaptive immune responses.

2006

Activation of dendritic cells by ligands for Toll-like receptors (TLR) is a crucial event in the initiation of innate and adaptive immune responses. Several classes of TLR ligands have been identified that interact with distinct members of the TLR-family. TLR4 ligands include lipopolysaccharide derived from different Gram-negative bacteria and viral proteins. Recent reports have demonstrated the TLR-mediated activation of dendritic cells by heat shock proteins (HSPs). However, doubts were raised as to what extent this effect was due to lipopolysaccharide contaminations of the HSP preparations. We re-examined this phenomenon using Gp96 or its N-terminal domain, nominally endotoxin-free (0.5 …

LipopolysaccharidesLipopolysaccharideBiologyCD8-Positive T-LymphocytesBiochemistrychemistry.chemical_compoundMiceImmune systemDogsHeat shock proteinAnimalsHumansReceptorMolecular BiologyInflammationMice Inbred BALB CInnate immune systemMembrane GlycoproteinsCCL18Cell BiologyToll-Like Receptor 2Cell biologyEndotoxinsMice Inbred C57BLToll-Like Receptor 4TLR2BiochemistrychemistryTLR4The Journal of biological chemistry
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