2022
Efficacy of Disease Modifying Therapies in Progressive MS and How Immune Senescence May Explain Their Failure
Manouchehri N, Salinas VH, Yeganeh N, Pitt D, Hussain RZ, Stuve O. Efficacy of Disease Modifying Therapies in Progressive MS and How Immune Senescence May Explain Their Failure. Frontiers In Neurology 2022, 13: 854390. PMID: 35432156, PMCID: PMC9009145, DOI: 10.3389/fneur.2022.854390.Peer-Reviewed Original ResearchProgressive multiple sclerosisSecondary progressive MSMultiple sclerosisImmune senescenceSecondary progressive multiple sclerosisDifferent MS phenotypesDisease-Modifying TherapiesSuccessful clinical managementAge-related factorsAdvent of diseaseModifying therapiesProgressive MSRelapse frequencyClinical managementImmune responseDistinct pathogenesesImmune systemM phenotypeDisease transitionTherapyMain correlatesDisease phenotypePatientsRRMSSignal changes
2018
Enhanced astrocyte responses are driven by a genetic risk allele associated with multiple sclerosis
Ponath G, Lincoln MR, Levine-Ritterman M, Park C, Dahlawi S, Mubarak M, Sumida T, Airas L, Zhang S, Isitan C, Nguyen TD, Raine CS, Hafler DA, Pitt D. Enhanced astrocyte responses are driven by a genetic risk allele associated with multiple sclerosis. Nature Communications 2018, 9: 5337. PMID: 30559390, PMCID: PMC6297228, DOI: 10.1038/s41467-018-07785-8.Peer-Reviewed Original ResearchConceptsMultiple sclerosisAstrocyte responseRisk variantsLocal autoimmune inflammationPeripheral immune cellsCentral nervous system cellsPeripheral immune systemCultured human astrocytesNervous system cellsNF-κB signalingCNS accessDysfunctional lymphocytesAstroglial functionAutoimmune inflammationLymphocytic infiltrateLymphocyte recruitmentImmune cellsGenetic risk allelesGenetic risk variantsMS lesionsMS susceptibilityHuman astrocytesLesion sizeImmune systemSystem cells
2015
Analysis of miRNA in Normal Appearing White Matter to Identify Altered CNS Pathways in Multiple Sclerosis
Guerau-de-Arellano M, Liu Y, Meisen WH, Pitt D, Racke MK, Lovett-Racke AE. Analysis of miRNA in Normal Appearing White Matter to Identify Altered CNS Pathways in Multiple Sclerosis. Journal Of Autoimmune Disorders 2015, 1 PMID: 26894232, PMCID: PMC4755487, DOI: 10.21767/2471-8153.100006.Peer-Reviewed Original ResearchCNS pathwaysMS patientsNormal Appearing White MatterBlood-brain barrierMultiple sclerosis susceptibilityPatients' CNSCNS inflammationMultiple sclerosisNeuroprotective mechanismsPost-transcriptional dysregulationControl subjectsUnderlying dysregulationImmune systemWhite matterCNSInflammationMiR-191Target predicationNAWMMiRNA profiling studiesPatientsMRNA analysisMAPK pathwayGenetic contributorsPathway analysis
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