2014
Cell-selective knockout and 3D confocal image analysis reveals separate roles for astrocyte-and endothelial-derived CCL2 in neuroinflammation
Paul D, Ge S, Lemire Y, Jellison ER, Serwanski DR, Ruddle NH, Pachter JS. Cell-selective knockout and 3D confocal image analysis reveals separate roles for astrocyte-and endothelial-derived CCL2 in neuroinflammation. Journal Of Neuroinflammation 2014, 11: 10. PMID: 24444311, PMCID: PMC3906899, DOI: 10.1186/1742-2094-11-10.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisBlood-brain barrierCentral nervous systemBrain microvascular endothelial cellsKO miceEarly experimental autoimmune encephalomyelitisMyelin oligodendrocyte glycoprotein peptideEndothelial cellsNormal central nervous systemReduced EAE severityClinical disease progressionIFN-γ productionT cell proliferationWild-type miceMicrovascular endothelial cellsCCL2 immunoreactivityEAE severityImmunofluorescence confocal microscopyBBB damageEAE modelAutoimmune encephalomyelitisIL-17Neuroinflammatory conditionsNeuroinflammatory diseasesWT mice
2007
Regulatory T cells selectively protect against experimental autoimmune encephalomyelitis induced with self but not foreign antigens (B79)
Akirav E, Xu Y, Bergman C, Hill M, Ruddle N. Regulatory T cells selectively protect against experimental autoimmune encephalomyelitis induced with self but not foreign antigens (B79). The Journal Of Immunology 2007, 178: lb16-lb17. DOI: 10.4049/jimmunol.178.supp.b79.Peer-Reviewed Original ResearchMouse myelin oligodendrocyte glycoproteinExperimental autoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinRegulatory T cellsTreg depletionT cellsAutoimmune encephalomyelitisMultiple sclerosisHuman myelin oligodendrocyte glycoproteinRatio of IFNγT cell responsesT cell proliferationCentral nervous systemEAE severityMOG35-55IL17 productionAutoimmune diseasesOligodendrocyte glycoproteinForeign antigensMurine modelNervous systemRelated antigensDisease severityCell responsesMice
2001
Resident and Infiltrating Central Nervous System APCs Regulate the Emergence and Resolution of Experimental Autoimmune Encephalomyelitis
Juedes A, Ruddle N. Resident and Infiltrating Central Nervous System APCs Regulate the Emergence and Resolution of Experimental Autoimmune Encephalomyelitis. The Journal Of Immunology 2001, 166: 5168-5175. PMID: 11290800, DOI: 10.4049/jimmunol.166.8.5168.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntigen PresentationAntigen-Presenting CellsB7-1 AntigenBrainCell LineCell MovementDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFemaleGrowth InhibitorsHistocompatibility Antigens Class IHistocompatibility Antigens Class IILymphocyte ActivationMacromolecular SubstancesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMicrogliaMolecular Sequence DataMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNitric OxideSpinal CordT-LymphocytesConceptsExperimental autoimmune encephalomyelitisT cell proliferationT cellsT cell linesCNS APCCNS APCsAutoimmune encephalomyelitisMHC-IITarget organsInducible NO synthase-deficient miceT cell cytokine productionTh1 T cellsAutoreactive T cellsCell cytokine productionIFN-gamma productionB7-1 expressionSynthase-deficient miceCell proliferationMac-1 cellsCell linesInitiation of diseaseProduction of NOResident microgliaMyelin oligodendrocyteCytokine production