Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis
Saini H, Rifkin R, Gorelik M, Huang H, Ferguson Z, Jones M, Levy M. Passively transferred human NMO-IgG exacerbates demyelination in mouse experimental autoimmune encephalomyelitis. BMC Neurology 2013, 13: 104. PMID: 23927715, PMCID: PMC3750922, DOI: 10.1186/1471-2377-13-104.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, LyAquaporin 4Demyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansImmunoglobulin GMiceMice, Inbred C57BLMyelin SheathMyelin-Oligodendrocyte GlycoproteinNeuromyelitis OpticaOptic NervePeptide FragmentsSpinal CordTime FactorsConceptsNMO-IgGCentral nervous systemSpinal cordOptic nerveAquaporin-4Long-term clinical outcomesMouse experimental autoimmune encephalomyelitisNMO-IgG biomarkerAquaporin-4 water channelsExperimental autoimmune encephalomyelitisOutcome of miceSevere neurological disabilityOnset of diseaseBackgroundNeuromyelitis opticaClinical worseningHumoral inflammationLonger-term outcomesAutoimmune encephalomyelitisFrequent exacerbationsClinical outcomesInflammatory disordersClinical examContext of EAENeurological disabilityMice
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