Search results for "EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS"

showing 10 items of 88 documents

Reversible neural stem cell niche dysfunction in a model of multiple sclerosis

2011

Objective The subventricular zone (SVZ) of the brain constitutes a niche for neural stem and progenitor cells that can initiate repair after central nervous system (CNS) injury. In a relapsing-remitting model of experimental autoimmune encephalomyelitis (EAE), the neural stem cells (NSCs) become activated and initiate regeneration during acute disease, but lose this ability during the chronic phases of disease. We hypothesized that chronic microglia activation contributes to the failure of the NSC repair potential in the SVZ. Methods Using bromodeoxyuridine injections at different time points during EAE, we quantified the number of proliferating and differentiating progenitors, and evaluate…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisTime FactorsSubventricular zoneCell CountMinocyclineBiologyArticleMiceSOX2Microscopy Electron TransmissionNeural Stem CellsCell MovementmedicineSecondary PreventionAnimalsProgenitor cellStem Cell NicheMyelin Proteolipid ProteinCell ProliferationMicrogliaExperimental autoimmune encephalomyelitismedicine.diseaseNeural stem cellOligodendrocytePeptide FragmentsAnti-Bacterial Agentsnervous system diseasesDisease Models AnimalOligodendrogliamedicine.anatomical_structureNeurologyBromodeoxyuridinenervous systemNeurology (clinical)MicrogliaStem cellNeuroscience
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Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination.

2010

Abstract Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADDODC-KO). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADDODC-KO mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADDODC-KO mice followed an ameliorated clinical di…

Encephalomyelitis Autoimmune ExperimentalMultiple Sclerosisgenetic structuresEncephalomyelitisFas-Associated Death Domain ProteinImmunologyApoptosisurologic and male genital diseasesMiceConditional gene knockoutDemyelinating diseasemedicineImmunology and AllergyAnimalsFADDLymphocytesMyelin SheathDeath domainInflammationMice KnockoutbiologyMultiple sclerosisMacrophagesfungiExperimental autoimmune encephalomyelitismedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureGene Expression RegulationSpinal CordCancer researchbiology.proteinbiological phenomena cell phenomena and immunityGene DeletionJournal of immunology (Baltimore, Md. : 1950)
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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L-Selectin-deficient SJL and C57BL/6 mice are not resistant to experimental autoimmune encephalomyelitis

2008

L-selectin has been suggested to play a role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Here we demonstrate that L-selectin(-/-) SJL mice are susceptible to proteolipid protein (PLP)-induced EAE because the compromised antigen-specific T cell proliferation in peripheral lymph nodes is fully compensated by the T cell response raised in their spleen. Transfer of PLP-specific T cells into syngeneic recipients induced EAE independent of the presence or absence of L-selectin on PLP-specific T cells or in the recipient. Leukocyte infiltration into the central nervous system parenchyma was detectable independent of the mode of dis…

Encephalomyelitis Autoimmune ExperimentalProteolipid protein 1OvalbuminT cellImmunologySpleenPathogenesisMice03 medical and health sciencesMyelin0302 clinical medicineCell Movementimmune system diseasesmedicineAnimalsImmunology and AllergyL-SelectinMyelin Proteolipid Protein030304 developmental biologyInflammation0303 health sciencesbiologyExperimental autoimmune encephalomyelitismedicine.diseaseAdoptive TransferOligodendrocytenervous system diseases3. Good healthMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinFemaleL-selectinSpleen030215 immunologyEuropean Journal of Immunology
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Protection from experimental allergic encephalomyelitis by application of a bacterial superantigen

1992

Certain bacterial and viral T cell stimulating proteins ('superantigens') are known to be very potent activators of T cells with certain V beta receptors. When applied in vivo these molecules induce anergy in those T cells responding to them. In this study we have investigated the influence of staphylococcal enterotoxins (SE) on myelin basic protein (MBP)-specific T cells in Lewis rats. As MBP-specific T cells in rats belong exclusively to the V beta 8.2+ CD4+ subset, the induction of experimental allergic encephalomyelitis (EAE) allows for an estimation of the functional state of the respective V beta-bearing T cells after enterotoxin-induced activation. In vitro, various MBP-specific T ce…

Encephalomyelitis Autoimmune ExperimentalT-LymphocytesEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationCell LineImmune toleranceEnterotoxinsAntigenImmune TolerancemedicineSuperantigenAnimalsImmunology and AllergyAntigens BacterialExperimental autoimmune encephalomyelitisGeneral MedicineT lymphocytemedicine.diseaseRatsMyelin basic proteinmedicine.anatomical_structureRats Inbred LewImmunologybiology.proteinFemaleInternational Immunology
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Pre- and postsynaptic type-1 cannabinoid receptors control the alterations of glutamate transmission in experimental autoimmune encephalomyelitis

2013

Type-1 cannabinoid receptors (CB1R) are important regulators of the neurodegenerative damage in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). In GABAergic striatal neurons, CB1R stimulation exerts protective effects by limiting inflammation-induced potentiation of glutamate-mediated spontaneous excitatory postsynaptic currents (sEPSCs). Here we show that CB1R located on GABAergic or on glutamatergic neurons are differentially involved in the pre- and postsynaptic alterations of sEPSCs caused by EAE in the striatum. After induction of EAE, mice selectively lacking CB1R on GABAergic neurons (GABA-CB1R-KO) showed exacerbated alterations of sEPSC duration in GA…

Encephalomyelitis Autoimmune ExperimentalTime FactorsPostsynaptic CurrentPresynaptic TerminalsExcitotoxicityGlutamic AcidIn Vitro TechniquesBiologyMedium spiny neuronmedicine.disease_causeSynaptic TransmissionMiceCellular and Molecular NeuroscienceGlutamatergicReceptor Cannabinoid CB1Postsynaptic potentialmedicineAnimalsgamma-Aminobutyric AcidMice KnockoutNeuronsPharmacologyExperimental autoimmune encephalomyelitisGlutamate receptorExcitatory Postsynaptic Potentialsmedicine.diseaseCorpus StriatumMice Inbred C57BLnervous systemDisease ProgressionExcitatory postsynaptic potentialFemaleSettore MED/26 - NeurologiaNeuroscience
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Persistent inflammation alters the function of the endogenous brain stem cell compartment

2008

Endogenous neural stem/precursor cells (NPCs) are considered a functional reservoir for promoting tissue homeostasis and repair after injury, therefore regenerative strategies that mobilize these cells have recently been proposed. Despite evidence of increased neurogenesis upon acute inflammatory insults (e.g. ischaemic stroke), the plasticity of the endogenous brain stem cell compartment in chronic CNS inflammatory disorders remains poorly characterized. Here we show that persistent brain inflammation, induced by immune cells targeting myelin, extensively alters the proliferative and migratory properties of subventricular zone (SVZ)-resident NPCs in vivo leading to significant accumulation…

Encephalomyelitis Autoimmune Experimentalexperimental autoimmune encephalomyelitisSubventricular zoneInflammationBiologymultiple sclerosisMice03 medical and health sciences0302 clinical medicineNeuroblastCell MovementPrecursor cellischemic strokemedicineAnimalsCells CulturedTissue homeostasisCell Proliferationneural stem cells030304 developmental biology0303 health sciencesStem CellsCell CycleNeurogenesisOriginal Articlesbrain cell stemNeural stem cellClone CellsNerve RegenerationMice Inbred C57BLMicroscopy Electronneurogenesismedicine.anatomical_structureinflammationChronic DiseaseModels AnimalCytokinesFemaleNeurology (clinical)Stem cellmedicine.symptomNeuroscience030217 neurology & neurosurgeryBrain StemBrain
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IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+regulatory T cells

2008

The conditions leading to the induction of adaptive Foxp3+regulatory T cells (T-regs) from peripheral T cells in vivo are incompletely understood. Here, we show that unresponsiveness of T cells to IL-6 by T cell-selective deletion of gp130 or immunization of wild-type mice with antigen in incomplete Freund's adjuvant (IFA), which fails to induce IL-6, promotes the conversion of peripheral CD4+T cells into adaptive Foxp3+T-regs. Thus, both T cell-conditional gp130 knockout (KO) mice immunized with MOG35-55 in complete Freund's adjuvant (CFA) and wild-type mice immunized with MOG35-55 in IFA develop overwhelming antigen-specific T-reg responses and are protected from experimental autoimmune e…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentchemical and pharmacologic phenomenaInflammationBiologyT-Lymphocytes RegulatoryMiceInterleukin 21Antigenimmune system diseasesmedicineAnimalsCytotoxic T cellIL-2 receptorMice KnockoutMultidisciplinaryInterleukin-6Experimental autoimmune encephalomyelitisFOXP3Forkhead Transcription Factorshemic and immune systemsT-Lymphocytes Helper-InducerBiological Sciencesmedicine.diseaseCytokineImmunologymedicine.symptomProceedings of the National Academy of Sciences
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Treatment of experimental autoimmune encephalomyelitis with adenylate deaminase from Penicillium lanoso-viride.

2000

The effect of intramuscularly administered immunomodulator, adenylate deaminase (E.C. 3.5.4.6), from Penicillium lanoso-viride on the clinical score of acute experimental autoimmune encephalomyelitis (EAE), a T cell-mediated autoimmune disease, was examined by inoculation of guinea pigs with rabbit brain and spinal cord homogenate (encephalitogen) and complete Freund's adjuvant. Adenylate deaminase (ADA) was effective in delaying the onset of clinical disease. ADA inhibited the severity of EAE. There was a significant decrease in clinical signs. A decrease in the number of morbid and dead animals was observed. Of ADA treated animals, 50-80% developed no clinical manifestations of EAE. The o…

MaleEncephalomyelitis Autoimmune ExperimentalEncephalomyelitisImmunologyGuinea PigsCross Reactionsmedicine.disease_causeInjections IntramuscularAutoimmunityAMP DeaminaseMiceBlood serumAdjuvants Immunologicimmune system diseasesImmunology and AllergyMedicineAnimalsHypersensitivity DelayedComplement ActivationSkin TestsAutoimmune diseaseMice Inbred BALB Cbiologybusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisPenicilliumBrainAMP deaminasemedicine.diseaseSpinal CordImmunologybiology.proteinFemaleImmunizationRabbitsAntibodybusiness2'3'-Cyclic-Nucleotide PhosphodiesterasesJournal of autoimmunity
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BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions

2011

Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip® arrays. One finding was the predominance of immune a…

MalePathologyPlatelet-derived growth factormedicine.medical_treatmentCell CountBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineFluorescent Antibody Technique IndirectOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth Factor0303 health sciencesGlial fibrillary acidic proteinbiologyExperimental autoimmune encephalomyelitisAstrocytomaMiddle AgedImmunohistochemistrymedicine.anatomical_structureFemaleFibroblast Growth Factor 2Fatty Acid-Binding Protein 7Adultmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyBlotting WesternNerve Tissue ProteinsFatty Acid-Binding ProteinsReal-Time Polymerase Chain ReactionTransfection03 medical and health sciencesCuprizoneCell Line TumorGlial Fibrillary Acidic ProteinmedicineAnimalsHumansRNA MessengerRemyelination030304 developmental biologyAgedEndocrine and Autonomic SystemsMultiple sclerosisGrowth factorTumor Suppressor Proteinsmedicine.diseaseOligodendrocyteMice Inbred C57BLchemistryAstrocytesbiology.proteinOsteopontinCarrier Proteins030217 neurology & neurosurgeryDemyelinating Diseases
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