Search results for "Myelin-Oligodendrocyte Glycoprotein"

showing 9 items of 19 documents

Autoantibody depletion ameliorates disease in murine experimental autoimmune encephalomyelitis.

2013

Much data support a role for central nervous system antigen-specific antibodies in the pathogenesis of multiple sclerosis (MS). The effects of inducing a decrease in (auto)antibody levels on MS or experimental autoimmune encephalomyelitis (EAE) through specific blockade of FcRn, however, remain unexplored. We recently developed engineered antibodies that lower endogenous IgG levels by competing for binding to FcRn. These Abdegs ("antibodies that enhance IgG degradation") can be used to directly assess the effect of decreased antibody levels in inflammatory diseases. In the current study, we show that Abdeg delivery ameliorates disease in an EAE model that is antibody dependent. Abdegs could…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisShort CommunicationImmunologyCentral nervous systemCHO CellsReceptors FcBiologyProtein EngineeringImmunoglobulin GAntibodiesMyelin oligodendrocyte glycoproteinPathogenesisMiceCricetulusCricetinaemedicineImmunology and AllergyAnimalsHumansAutoantibodiesMultiple sclerosisExperimental autoimmune encephalomyelitisHistocompatibility Antigens Class IAutoantibodymedicine.diseaseRecombinant ProteinsMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GImmunologybiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinAntibodyProtein BindingmAbs
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Myelin-specific T cells also recognize neuronal autoantigen in a transgenic mouse model of multiple sclerosis

2008

T-cell recognition of autoantigens is important in the development of autoimmune disease. Now, Hartmut Wekerle and his colleagues demonstrate that organ-specific autoimmune responses may be driven by T cells that simultaneously respond to two different autoantigens found within the same target tissue. We describe here the paradoxical development of spontaneous experimental autoimmune encephalomyelitis (EAE) in transgenic mice expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell antigen receptor (TCR) in the absence of MOG. We report that in Mog-deficient mice (Mog−/−), the autoimmune response by transgenic T cells is redirected to a neuronal cytoskeletal self antigen, neur…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT-LymphocytesMolecular Sequence DataReceptors Antigen T-CellMice TransgenicCross ReactionsMajor histocompatibility complexAutoantigensGeneral Biochemistry Genetics and Molecular BiologyEpitopeMyelin oligodendrocyte glycoproteinMice03 medical and health sciencesMyelin0302 clinical medicineAntigenNeurofilament ProteinsAnimalsMedicineAmino Acid SequenceMyelin Sheath030304 developmental biologyAutoimmune disease0303 health sciencesbiologybusiness.industryExperimental autoimmune encephalomyelitisT-cell receptorGeneral Medicinemedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalMyelin-Associated Glycoproteinmedicine.anatomical_structureImmunologybiology.proteinMyelin-Oligodendrocyte GlycoproteinbusinessMyelin Proteins030215 immunologyNature Medicine
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IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice

2009

The clear association of Th17 cells with autoimmune pathogenicity implicates Th17 cytokines as critical mediators of chronic autoimmune diseases such as EAE. To study the impact of IL-17A on CNS inflammation, we generated transgenic mice in which high levels of expression of IL-17A could be initiated after Cre-mediated recombination. Although ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell–specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice. In the context of EAE, neither the T cell–driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease. Sin…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentT cellEncephalomyelitisPopulation610 Medicine & healthMice TransgenicInflammation2700 General Medicine10263 Institute of Experimental ImmunologyMyelin oligodendrocyte glycoproteinMicemedicineAnimalseducationCells CulturedGlycoproteinseducation.field_of_studybiologybusiness.industryInterleukin-17General MedicineTh1 Cellsmedicine.diseasePeptide FragmentsMice Inbred C57BLCytokinemedicine.anatomical_structureImmunologybiology.protein570 Life sciences; biologyExperimental pathologyFemaleMyelin-Oligodendrocyte GlycoproteinInterleukin 17medicine.symptombusinessGranulocytesResearch Article
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Upregulation of antibody response to heat shock proteins and tissue antigens in an ocular ischemia model.

2011

PURPOSE. The aim of this study was to characterize the serum antibody reactivities occurring after ocular ischemia reperfusion. The time course of serum antibody responses was examined. METHODS. Wistar rats were exposed to transient ocular ischemia by elevating intraocular pressure to 130 mm Hg for 60 minutes. Axonal damage was evaluated on optic-nerve sections 2 and 4 weeks later. Blood samples collected before and several times after ischemia were used for antibody detection via customized protein microarrays. Different tissue antigens, including heat shock proteins (HSPs) and crystallins, were selected based on previous identification of antibody reactivities in studies on ischemic event…

MalePathologymedicine.medical_specialtyIschemiaHSP27 Heat-Shock ProteinsProtein Array AnalysisVimentinBiologyAutoantigensDownregulation and upregulationAntigenRetinal DiseasesHeat shock proteinGlial Fibrillary Acidic ProteinmedicineAnimalsRats WistarEye ProteinsIntraocular PressureAutoantibodiesGlial fibrillary acidic proteinRetinal VesselsSpectrinMyelin Basic ProteinOptic Nervemedicine.diseaseAxonsRatsUp-RegulationMyelin-Associated GlycoproteinShock (circulatory)Immunoglobulin GReperfusion Injurybiology.proteinMyelin-Oligodendrocyte Glycoproteinmedicine.symptomAntibodyMyelin ProteinsInvestigative ophthalmologyvisual science
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Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
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Peroxisomal and mitochondrial status of two murine oligodendrocytic cell lines (158N, 158JP): potential models for the study of peroxisomal disorders…

2009

International audience; In some neurodegenerative disorders (leukodystrophies) characterized by myelin alterations, the defect of peroxisomal functions on myelin-producing cells (oligodendrocytes) are poorly understood. The development of in vitro models is fundamental to understanding the physiopathogenesis of these diseases. We characterized two immortalized murine oligodendrocyte cell lines: a normal (158N) and a jimpy (158JP) cell line mutated for the proteolipid protein PLP/DM20. Fluorescence microscopy, flow cytometry, and western blotting analysis allow to identify major myelin proteins (PLP colocalizing with mitochondria; myelin basic protein), oligodendrocyte (CNPase and myelin oli…

Proteolipid protein 1BiochemistryMiceMyelinMESH : PhenylbutyratesperoxisomeIsomerasesMESH : Myelin Basic ProteinsEnoyl-CoA HydrataseCell Line TransformedUltrasonographybiologyMESH : Gene Expression RegulationMESH : Myelin Proteolipid Protein3-Hydroxyacyl CoA DehydrogenasesMESH : Myelin-Associated GlycoproteinMESH : Cell Line TransformedPeroxisomeMESH : Multienzyme ComplexesMESH : OligodendrogliaMESH : Enoyl-CoA HydrataseCatalaseFlow CytometryMESH : 3-Hydroxyacyl CoA DehydrogenasesPhenylbutyratesmitochondriaMyelin-Associated GlycoproteinOligodendrogliamyelinMESH : Antineoplastic Agentsmedicine.anatomical_structureMESH : Microscopy Electron TransmissionBiochemistryACOX1MESH : MitochondriaMESH : Acyl-CoA Oxidase2'3'-Cyclic-Nucleotide PhosphodiesterasesMESH : IsomerasesOxidation-ReductionMyelin ProteinsMESH : Flow CytometryAntineoplastic AgentsPeroxisomal Bifunctional EnzymeStatistics NonparametricMyelin oligodendrocyte glycoproteinCellular and Molecular NeuroscienceMicroscopy Electron TransmissionMultienzyme ComplexesMESH : CatalaseMESH : MicePeroxisomesmedicineAnimalsMESH : ATP-Binding Cassette TransportersMyelin Proteolipid ProteinMESH : Statistics Nonparametric[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Oxidation-ReductionMyelin Basic Proteinmurine oligodendrocytesMESH : 2'3'-Cyclic-Nucleotide PhosphodiesterasesPeroxisomal transportOligodendrocyteMyelin basic proteinGene Expression Regulationbiology.proteinATP-Binding Cassette TransportersMyelin-Oligodendrocyte GlycoproteinAcyl-CoA OxidaseMESH : AnimalsMESH : Peroxisomes
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Distinct endocytic recycling of myelin proteins promotes oligodendroglial membrane remodeling.

2008

The central nervous system myelin sheath is a multilayered specialized membrane with compacted and non-compacted domains of defined protein composition. How oligodendrocytes regulate myelin membrane trafficking and establish membrane domains during myelination is largely unknown. Oligodendroglial cells respond to neuronal signals by adjusting the relative levels of endocytosis and exocytosis of the major myelin protein, proteolipid protein (PLP). We investigated whether endocytic trafficking is common to myelin proteins and analyzed the endocytic fates of proteins with distinct myelin subdomain localization. Interestingly, we found that PLP, myelin-associated glycoprotein (MAG) and myelin-o…

Proteolipid protein 1Endocytic cycleCell MembraneEndocytic recyclingCell BiologyBiologyEndocytosisExocytosisEndocytosisCell biologyMyelin oligodendrocyte glycoproteinMyelinMiceMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structurenervous systemimmune system diseasesCompact myelinmedicinebiology.proteinAnimalsMyelin-Oligodendrocyte GlycoproteinMyelin Proteolipid ProteinMyelin ProteinsJournal of cell science
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Preclinical Retinal Neurodegeneration in a Model of Multiple Sclerosis

2012

Neurodegeneration plays a major role in multiple sclerosis (MS), in which it is thought to be the main determinant of permanent disability. However, the relationship between the immune response and the onset of neurodegeneration is still a matter of debate. Moreover, recent findings in MS patients raised the question of whether primary neurodegenerative changes can occur in the retina independent of optic nerve inflammation. Using a rat model of MS that frequently leads to optic neuritis, we have investigated the interconnection between neurodegenerative and inflammatory changes in the retina and the optic nerves with special focus on preclinical disease stages. We report that, before manif…

Retinal Ganglion CellsPathologyTime FactorsStilbamidinesgenetic structuresJournal ClubFreund's Adjuvantchemistry.chemical_compoundBlood-Retinal BarrierStudent’s SectionCell DeathMicrogliabiologyGeneral NeuroscienceRetinal DegenerationNeurodegenerationArticlesmedicine.anatomical_structureSpinal CordRetinal ganglion cellOptic nerveFemaleMicrogliaMyelin Proteinsmedicine.medical_specialtyMultiple SclerosisEnzyme-Linked Immunosorbent AssayRetinaMyelin oligodendrocyte glycoproteinMicroscopy Electron TransmissionAntigens CDOccludinGlial Fibrillary Acidic ProteinIn Situ Nick-End LabelingmedicineAnimalsOptic neuritisAquaporin 4Retinabusiness.industryMacrophagesMultiple sclerosisMembrane ProteinsRetinalOptic Nervemedicine.diseaseeye diseasesRatsDisease Models Animalchemistrybiology.proteinMyelin-Oligodendrocyte Glycoproteinsense organsbusinessNeuroscienceThe Journal of Neuroscience
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Protein kinase CK2 governs the molecular decision between encephalitogenic T H 17 cell and T reg cell development

2016

T helper 17 (TH17) cells represent a discrete TH cell subset instrumental in the immune response to extracellular bacteria and fungi. However, TH17 cells are considered to be detrimentally involved in autoimmune diseases like multiple sclerosis (MS). In contrast to TH17 cells, regulatory T (Treg) cells were shown to be pivotal in the maintenance of peripheral tolerance. Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising target for treating autoimmune diseases. However, the molecular mechanisms controlling this balance are still unclear. Here, we report that pharmacological inhibition as well as genetic ablat…

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisCellMice Transgenicchemical and pharmacologic phenomenaBiologySeverity of Illness IndexT-Lymphocytes RegulatoryMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansIL-2 receptorPhosphorylationCasein Kinase IISTAT3MultidisciplinaryCell growthInterleukin-17Experimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorFOXP3Peripheral toleranceForkhead Transcription Factorshemic and immune systemsReceptors Interleukinmedicine.diseasePeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationImmunologybiology.proteinCancer researchTh17 CellsMyelin-Oligodendrocyte GlycoproteinSignal Transduction030215 immunologyProceedings of the National Academy of Sciences
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