0000000000801511

AUTHOR

Josef Priller

showing 5 related works from this author

CD14 is a key organizer of microglial responses to CNS infection and injury

2015

Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced …

0301 basic medicineChemokineToll-like receptorInnate immune systembiologyMicrogliaCD14Proinflammatory cytokine03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structureImmune systemNeurologyImmunologybiology.proteinTLR4medicineGlia
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RNA Sequencing of Human Peripheral Blood Cells Indicates Upregulation of Immune-Related Genes in Huntington's Disease

2020

Huntington's disease (HD) is an autosomal dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the Huntingtin gene. As disease-modifying therapies for HD are being developed, peripheral blood cells may be used to indicate disease progression and to monitor treatment response. In order to investigate whether gene expression changes can be found in the blood of individuals with HD that distinguish them from healthy controls, we performed transcriptome analysis by next-generation sequencing (RNA-seq). We detected a gene expression signature consistent with dysregulation of immune-related functions and inflammatory response in peripheral blood from HD ca…

inflammationHuntington's diseaseRNA-Seqdifferential gene expressiondisease markerslcsh:Neurology. Diseases of the nervous systemlcsh:RC346-429Frontiers in Neurology
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Intrahippocampal transplantation of mesenchymal stromal cells promotes neuroplasticity

2012

Multipotent mesenchymal stromal cells (MSC) secrete soluble factors that stimulate the surrounding microenvironment. Such paracrine effects might underlie the potential benefits of many stem cell therapies. We tested the hypothesis that MSC are able to enhance intrinsic cellular plasticity in the adult rat hippocampus.Rat bone marrow-derived MSC were labeled with very small superparamagnetic iron oxide particles (VSOP), which allowed for non-invasive graft localization by magnetic resonance imaging (MRI). Moreover, MSC were transduced with lentiviral vectors to express the green fluorescent protein (GFP). The effects of bilateral MSC transplantation on hippocampal cellular plasticity were a…

Cancer ResearchCell SurvivalImmunologyCell- and Tissue-Based TherapyBone Marrow CellsCitalopramHippocampal formationBiologyMesenchymal Stem Cell TransplantationFerric CompoundsHippocampusGreen fluorescent proteinParacrine signallingAnimalsImmunology and AllergyGenetics (clinical)Cell ProliferationTransplantationNeuronal PlasticityCell growthMesenchymal stem cellNeurogenesisMesenchymal Stem CellsCell BiologyAnatomyMagnetic Resonance ImagingRatsCell biologyTransplantationOncologyStem cellCytotherapy
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IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous system

2011

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by …

Central Nervous SystemBlotting WesternIκB kinaseBiologyddc:616.07Myelin assemblyMicroglia/cytology/metabolismNerve Regeneration/physiologyDemyelinating Diseases/chemically induced/metabolism03 medical and health sciencesMyelinCuprizoneMice0302 clinical medicineCentral Nervous System/cytology/metabolismmedicineAnimalsRemyelinationCHUKMyelin Sheath030304 developmental biologyAstrocytes/cytology/metabolismMyelin Sheath/metabolism0303 health sciencesReverse Transcriptase Polymerase Chain ReactionSignal Transduction/physiologyI-Kappa-B KinaseNF-kappa BI-kappa B Kinase/metabolismOriginal ArticlesOligodendrocyte3. Good healthCell biologyI-kappa B KinaseNerve RegenerationOligodendrogliamedicine.anatomical_structureOligodendroglia/metabolismAstrocytesNF-kappa B/metabolismNeurogliaNeurology (clinical)MicrogliaNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesSignal Transduction
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IκB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-κB in the central nervous system

2017

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by …

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