2018
Myeloid cell plasticity in the evolution of central nervous system autoimmunity
Giles DA, Washnock‐Schmid J, Duncker PC, Dahlawi S, Ponath G, Pitt D, Segal BM. Myeloid cell plasticity in the evolution of central nervous system autoimmunity. Annals Of Neurology 2018, 83: 131-141. PMID: 29283442, PMCID: PMC5876132, DOI: 10.1002/ana.25128.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArginaseAutoimmune Diseases of the Nervous SystemBone Marrow CellsCell PlasticityChimeraDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalHumansImmunohistochemistryLectins, C-TypeMannose ReceptorMannose-Binding LectinsMiceMice, Inbred C57BLMultiple SclerosisMyeloid CellsNitric Oxide Synthase Type IIPhenotypeReceptors, Cell SurfaceConceptsInducible nitric oxide synthaseExperimental autoimmune encephalomyelitisCNS myeloid cellsCentral nervous systemCentral nervous system autoimmunityChronic active MS lesionsActive MS lesionsMultiple sclerosisMyeloid cellsMS lesionsAnimal model experimental autoimmune encephalomyelitisRemission of EAEModel experimental autoimmune encephalomyelitisMyeloid cell plasticityEncephalitogenic T cellsNitric oxide synthaseMyeloid cell phenotypeFuture therapeutic strategiesHuman myeloid cellsAnn NeurolNoninflammatory phenotypePolarized subsetsClinical remissionAutoimmune encephalomyelitisProinflammatory markers
2009
Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity
Pitt D, Gonzales E, Cross AH, Goldberg MP. Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity. Brain Research 2009, 1309: 146-154. PMID: 19896473, PMCID: PMC7343376, DOI: 10.1016/j.brainres.2009.10.066.Peer-Reviewed Original ResearchMeSH KeywordsAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsBiomarkersBrainDisease Models, AnimalExcitatory Amino Acid AgonistsFemaleHereditary Central Nervous System Demyelinating DiseasesLuminescent ProteinsMiceMice, Inbred C57BLMice, Neurologic MutantsMovement DisordersMyelin Basic ProteinNerve DegenerationNerve Fibers, MyelinatedNeurotoxinsN-MethylaspartateReceptors, AMPAConceptsNMDA receptorsShiverer miceAMPA/kainate receptorsLumbar dorsal columnWhite matter injuryWidespread axonal degenerationSpinal cord axonsActivation of receptorsReceptor-mediated toxicitySubset of axonsMyelin basic proteinAxonal vulnerabilityNeuroprotective therapiesGlutamate excitotoxicityNMDA injectionAxonal degenerationAxonal injuryDorsal columnsRotarod performanceAxon damageGlutamate toxicityCentral axonsGlial cellsS-AMPAAxonal toxicity
2003
Experimental Autoimmune Encephalomyelitis (EAE) in CCR2−/− Mice Susceptibility in Multiple Strains
Gaupp S, Pitt D, Kuziel WA, Cannella B, Raine CS. Experimental Autoimmune Encephalomyelitis (EAE) in CCR2−/− Mice Susceptibility in Multiple Strains. American Journal Of Pathology 2003, 162: 139-150. PMID: 12507897, PMCID: PMC1851120, DOI: 10.1016/s0002-9440(10)63805-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DivisionCrosses, GeneticDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalGenetic Predisposition to DiseaseGlycoproteinsImmunity, InnateImmunohistochemistryIn Situ HybridizationLymphocytesMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutMyelin SheathMyelin-Oligodendrocyte GlycoproteinNuclease Protection AssaysPeptide FragmentsReceptors, CCR2Receptors, ChemokineRNA, MessengerSpecies SpecificityConceptsExperimental autoimmune encephalomyelitisCentral nervous systemAutoimmune encephalomyelitisLow molecular weight cytokinesLack of CCR2Deletion of CCR2Sites of inflammationWild-type animalsDifferent mouse strainsCCR2 deletionCNS lesionsMultiple sclerosisWeight cytokinesAutoimmune diseasesMouse susceptibilityNervous systemImmune systemCompensatory mechanismsBalb CCCR2Mouse strainsChemokinesMonocytesEncephalomyelitisAppropriate receptors
2000
Insulin-Like Growth Factor-1 Fails to Enhance Central Nervous System Myelin Repair during Autoimmune Demyelination
Cannella B, Pitt D, Capello E, Raine C. Insulin-Like Growth Factor-1 Fails to Enhance Central Nervous System Myelin Repair during Autoimmune Demyelination. American Journal Of Pathology 2000, 157: 933-943. PMID: 10980132, PMCID: PMC1885703, DOI: 10.1016/s0002-9440(10)64606-8.Peer-Reviewed Original ResearchConceptsInsulin-like growth factor-1Experimental autoimmune encephalomyelitisCentral nervous system tissueGrowth factor-1Nervous system tissueAcute phaseChronic phaseChronic time pointsTime pointsVehicle-treated groupIGF-1 administrationVehicle-treated controlsFactor 1Oligodendrocyte progenitor populationClinical ameliorationAutoimmune encephalomyelitisCytokine levelsDifferent time pointsTreatment regimenAutoimmune demyelinationMultiple sclerosisSJL miceMyelin regenerationMyelin repairTGF-beta2Glutamate excitotoxicity in a model of multiple sclerosis
Pitt D, Werner P, Raine C. Glutamate excitotoxicity in a model of multiple sclerosis. Nature Medicine 2000, 6: 67-70. PMID: 10613826, DOI: 10.1038/71555.Peer-Reviewed Original ResearchConceptsGlutamate excitotoxicityMultiple sclerosisAMPA/kainate antagonist NBQXAMPA/kainate typeCentral nervous system inflammationAMPA/kainate antagonistAntigen-primed T cellsCentral nervous system2Nervous system inflammationExperimental autoimmune encephalomyelitisCentral nervous systemMyelin-producing cellsLack of effectDemyelinating modelKainate typeSystem inflammationAutoimmune encephalomyelitisInflammatory attacksKainate antagonistAntagonist NBQXAutoimmune demyelinationPathologic featuresClinical differencesReceptor damageOligodendrocyte survivalGlutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?
Werner P, Pitt D, Raine CS. Glutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis? Journal Of Neural Transmission. Supplementa 2000, 375-385. PMID: 11205156, DOI: 10.1007/978-3-7091-6301-6_27.Peer-Reviewed Original ResearchConceptsCentral nervous systemAMPA/kainate antagonistMultiple sclerosisGlutamate excitotoxicityImmune cellsKainate antagonistAxonal damageAntigen-primed T cellsMyelin-producing cellsLack of effectSite of entryCNS inflammationInflammatory attacksExperimental autoimmunePerivascular cuffsAutoimmune demyelinationInflammatory lesionsClinical differencesOligodendrocyte survivalEffective therapyGlutamate receptorsOligodendrocyte deathT cellsExcitotoxicityLesion size