Search results for " EXPERIMENTAL"

showing 10 items of 3530 documents

Targeting CD52 does not affect murine neuron and microglia function.

2020

The humanized anti-CD52 antibody alemtuzumab is successfully used in the treatment of multiple sclerosis (MS) and is thought to exert most of its therapeutic action by depletion and repopulation of mainly B and T lymphocytes. Although neuroprotective effects of alemtuzumab have been suggested, direct effects of anti-CD52 treatment on glial cells and neurons within the CNS itself have not been investigated so far. Here, we show CD52 expression in murine neurons, astrocytes and microglia, both in vitro and in vivo. As expected, anti CD52-treatment caused profound lymphopenia and improved disease symptoms in mice subjected to experimental autoimmune encephalomyelitis (EAE). CD52 blockade also …

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCD52Excitotoxicitymedicine.disease_causeNeuroprotection03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsAlemtuzumabPharmacologyNeuronsMicrogliabusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.disease030104 developmental biologymedicine.anatomical_structureCD52 AntigenGene Expression RegulationAlemtuzumabCalciumNeuronMicrogliabusinessNeuroscience030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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Dendritic cells tip the balance towards induction of regulatory T cells upon priming in experimental autoimmune encephalomyelitis

2016

Counter-balancing regulatory mechanisms, such as the induction of regulatory T cells (Treg), limit the effects of autoimmune attack in neuroinflammation. However, the role of dendritic cells (DCs) as the most powerful antigen-presenting cells, which are intriguing therapeutic targets in this context, is not fully understood. Here, we demonstrate that conditional ablation of DCs during the priming phase of myelin-specific T cells in experimental autoimmune encephalomyelitis (EAE) selectively aborts inducible Treg (iTreg) induction, whereas generation of T helper (Th)1/17 cells is unaltered. DCs facilitate iTreg induction by creating a milieu with high levels of interleukin (IL)-2 due to a st…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalImmunologyMedizinPriming (immunology)chemical and pharmacologic phenomenaAutoimmunitymedicine.disease_causeLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmunityImmunomodulation03 medical and health sciencesMice0302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsNeuroinflammationCD40biologyMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukinhemic and immune systemsDendritic Cellsmedicine.disease030104 developmental biologyImmunologybiology.proteinInterleukin 12CytokinesTh17 Cells030217 neurology & neurosurgery
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EBI2 – Sensor for dihydroxycholesterol gradients in neuroinflammation

2018

Dihydroxycholesterols such as 7α,25-dihydroxysterols (7α,25-OHC) and 7α,27-OHC are generated from cholesterol by the enzymes CH25H, CYP7B1 and CYP27A1 in steady state but also in the context of inflammation. The G-protein coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2), also known as GPR183, senses these oxysterols and induces chemotactic migration of immune cells towards higher concentrations of these ligands. We recently showed that these ligands are upregulated in the CNS in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis and that EBI2 enhanced early infiltration of encephalitogenic T cells into the CNS. In this short-review we dis…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisInflammationContext (language use)BiochemistryReceptors G-Protein-Coupled03 medical and health sciencesImmune systemmedicineAnimalsHumansReceptorNeuroinflammationInflammationImmunity CellularChemistryChemotaxisExperimental autoimmune encephalomyelitisGPR183ChemotaxisGeneral Medicinemedicine.diseaseHydroxycholesterolsCell biologyDisease Models Animal030104 developmental biologymedicine.symptomBiochimie
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Graph Theoretical Framework of Brain Networks in Multiple Sclerosis: A Review of Concepts.

2019

Abstract Network science provides powerful access to essential organizational principles of the human brain. It has been applied in combination with graph theory to characterize brain connectivity patterns. In multiple sclerosis (MS), analysis of the brain networks derived from either structural or functional imaging provides new insights into pathological processes within the gray and white matter. Beyond focal lesions and diffuse tissue damage, network connectivity patterns could be important for closely tracking and predicting the disease course. In this review, we describe concepts of graph theory, highlight novel issues of tissue reorganization in acute and chronic neuroinflammation an…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisModels NeurologicalNetwork science03 medical and health sciences0302 clinical medicineNeural PathwaysmedicineAnimalsHumansGeneral NeuroscienceMultiple sclerosisBrainGraph theoryHuman brainmedicine.diseaseFunctional imaging030104 developmental biologymedicine.anatomical_structureGraph (abstract data type)DisconnectionPsychologyNeuroscience030217 neurology & neurosurgeryNetwork analysisNeuroscience
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Gatekeeper role of brain antigen‐presenting CD11c + cells in neuroinflammation

2015

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesAntigen-Presenting CellsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInterleukin 210302 clinical medicineCell MovementAnimalsCytotoxic T cellAntigen-presenting cellMolecular BiologyNeuroinflammationInterleukin 3CD40General Immunology and MicrobiologybiologyGeneral NeuroscienceInterleukin-17BrainGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsDendritic CellsArticlesNatural killer T cellCD11c AntigenMice Inbred C57BL030104 developmental biologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunologyThe EMBO Journal
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TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

2017

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8(+)CD103(+) DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune ence…

0301 basic medicineEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentCellular differentiationAutoimmunitychemical and pharmacologic phenomenaCD8-Positive T-LymphocytesBiologyT-Lymphocytes RegulatorySmad7 ProteinImmune toleranceMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmune TolerancemedicineAnimalsIndoleamine-Pyrrole 23-DioxygenaseMultidisciplinaryintegumentary systemExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsDendritic CellsDendritic cellTransforming growth factor betamedicine.diseaseCell biologyMice Inbred C57BLTolerance inductionBasic-Leucine Zipper Transcription Factors030104 developmental biologyCytokinePNAS PlusInterferon Regulatory FactorsImmunologybiology.proteinCytokinesSpleenCD8Signal Transduction030215 immunology
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Role of the epigenetic factor Sirt7 in neuroinflammation and neurogenesis.

2017

Epigenetic regulators are increasingly recognized as relevant modulators in the immune and nervous system. The class of sirtuins consists of NAD+-dependent histone deacetylases that regulate transcription. Sirtuin family member Sirt1 has already been shown to influence the disease course in an animal model of autoimmune neuroinflammation (experimental autoimmune encephalomyelitis (EAE). A role of Sirt7, a related epigenetic regulator, on immune system regulation has been proposed before, as these mice are more susceptible to develop inflammatory cardiomyopathy. Sirt7-/- animals showed no differences in clinical score compared to wild-type littermates after EAE induction with myelin oligoden…

0301 basic medicineEpigenetic regulation of neurogenesisEncephalomyelitis Autoimmune ExperimentalNeurogenesisAdaptive ImmunityHippocampusT-Lymphocytes RegulatoryMyelin oligodendrocyte glycoproteinEpigenesis Genetic03 medical and health sciencesImmune systemmedicineAnimalsSirtuinsNeuroinflammationCell ProliferationMice KnockoutNeuronsbiologyGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisGeneral Medicinemedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyImmunologySirtuinbiology.proteinEncephalitisFemaleNeuroscienceNeuroscience research
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IL-17A mediated endothelial breach promotes metastasis formation

2015

Abstract The role of the IL23/IL17A axis in tumor–immune interactions is a matter of controversy. Although some suggest that IL17A-producing T cells (TH17) can suppress tumor growth, others report that IL17A and IL23 accelerate tumor growth. Here, we systematically assessed the impact of IL17A-secreting lymphocytes in several murine models of tumor lung metastasis. Genetic fate mapping revealed that IL17A was secreted within lung metastases predominantly by γδ T cells, whereas TH17 cells were virtually absent. Using different tumor models, we found Il17a−/− mice to consistently develop fewer pulmonary tumor colonies. IL17A specifically increased blood vessel permeability and the expression …

0301 basic medicineGenetically modified mouseCancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsEndotheliumImmunologyMelanoma ExperimentalVascular permeability610 Medicine & healthBiology10263 Institute of Experimental ImmunologyCapillary Permeability03 medical and health sciencesCarcinoma Lewis LungCell Line TumormedicineCell AdhesionAnimals1306 Cancer ResearchCell adhesionMice Knockout2403 ImmunologyLungMelanomaInterleukin-17Transendothelial and Transepithelial MigrationEndothelial Cellsmedicine.diseaseMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureCell culture570 Life sciences; biologyInterleukin 17Endothelium VascularNeoplasm Transplantation
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Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia.

2021

Background:\ud \ud This cross-sectional study aimed to examine associations between excessive daytime sleepiness (EDS) with falls and falls related conditions in older adults.\ud \ud Methods:\ud \ud To assess EDS, the Epworth Sleepiness Scale was used, with a score of ≥11/24 points indicating EDS. Number of falls and fall history (at least one) in the last year were recorded. Timed Up and Go test (TUG) was used to assess fall risk. Sarcopenia was defined by SARC-F tool. A grip strength score of the dominant hand, measured with a hand-grip dynamometer, less than 16 kg in females and 27 kg in males was accepted as dynapenia. Frailty status was defined by five dimensions including shrinking, e…

0301 basic medicineGerontologyMaleAgingSarcopeniaExcessive daytime sleepinessTimed Up and Go testDisorders of Excessive SomnolenceBiochemistry03 medical and health sciencesGrip strength0302 clinical medicineEndocrinologyGeneticsmedicineHumansMolecular BiologyGeriatric AssessmentPostural BalanceDepression (differential diagnoses)AgedPolypharmacyAged 80 and overbusiness.industryEpworth Sleepiness ScaleCell Biologymedicine.disease030104 developmental biologyCross-Sectional StudiesSarcopeniaDynapenia Excessive daytime sleepiness FallsFrailty SarcopeniaTime and Motion StudiesSoysal P. Smith L. Tan S. G. Capar E. Veronese N. Yang L. -Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia.- Experimental gerontology ss.111364 2021Soysal P. Smith L. Tan S. G. Capar E. Veronese N. Yang L. -Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia- 17 th EuGMS Athens Yunanistan 11 - 13 Ekim 2021 ss.3-4Marital statusAccidental FallsFemalemedicine.symptombusinesshuman activities030217 neurology & neurosurgeryExperimental gerontology
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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