Search results for "Myelin oligodendrocyte glycoprotein"

showing 7 items of 17 documents

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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Modeling a complex disease: Multiple sclerosis—Update 2020

2021

Multiple sclerosis (MS) is a complex inflammatory disease of the central nervous system (CNS) with an unknown etiology. Thereby, MS is not a uniform disease but rather represents a spectrum of disorders, where each aspect needs to be modeled with specific requirements-for a systematic overview see our previous issue of this review (Kurschus, Wortge, & Waisman, 2011). However, there is broad consensus about the critical involvement of the immune system in the disease pathogenesis. To better understand how the immune system contributes to CNS autoimmunity, the model of experimental autoimmune encephalomyelitis (EAE) was developed. EAE can be induced in susceptible animals in many different wa…

Multiple sclerosisCentral nervous systemExperimental autoimmune encephalomyelitisComplex diseaseDiseaseBiologyDisease pathogenesismedicine.diseaseMyelin oligodendrocyte glycoprotein03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureImmune systemmedicinebiology.proteinNeuroscience030215 immunology
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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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Oligodendrocytes secrete exosomes containing major myelin and stress-protective proteins: Trophic support for axons?

2007

Oligodendrocytes synthesize the CNS myelin sheath by enwrapping axonal segments with elongations of their plasma membrane. Spatial and temporal control of membrane traffic is a prerequisite for proper myelin formation. The major myelin proteolipid protein (PLP) accumulates in late endosomal storage compartments and multivesicular bodies (MVBs). Fusion of MVBs with the plasma membrane results in the release of the intralumenal vesicles, termed exosomes, into the extracellular space. Here, we show that cultured oligodendrocytes secrete exosomes carrying major amounts of PLP and 2'3'-cyclic-nucleotide-phosphodiesterase (CNP). These exosomes migrated at the characteristic density of 1.10-1.14 g…

Proteolipid protein 1EndosomeClinical BiochemistryBiologyExosomeMicrovesiclesMyelin proteolipid proteinCell biologyMyelin oligodendrocyte glycoproteinMyelin basic proteinMyelinmedicine.anatomical_structurenervous systemBiochemistrybiology.proteinmedicineProteomics. Clinical applications
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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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Clinical and MRI measures to identify non-acute MOG-antibody disease in adults

2022

Abstract MRI and clinical features of myelin oligodendrocyte glycoprotein (MOG)-antibody disease may overlap with those of other inflammatory demyelinating conditions posing diagnostic challenges, especially in non-acute phases and when serologic testing for MOG antibodies is unavailable or shows uncertain results. We aimed to identify MRI and clinical markers that differentiate non-acute MOG-antibody disease from aquaporin 4 (AQP4)-antibody neuromyelitis optica spectrum disorder and relapsing remitting multiple sclerosis, guiding in the identification of patients with MOG-antibody disease in clinical practice. In this cross-sectional retrospective study, data from 16 MAGNIMS centres were i…

aquaporin 4-antibody positive neuromyelitis optica spectrum disorder; differential diagnosis; imaging; multiple sclerosis; myelin oligodendrocyte glycoprotein antibody-associated diseaseaquaporin 4-antibody positive neuromyelitis optica spectrum disordermyelin oligodendrocyte glycoprotein antibody-associated diseasedifferential diagnosisimagingNeurology (clinical)multiple sclerosis
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