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
2012
Tertiary lymphoid organ development coincides with determinant spreading of the myelin-specific T cell response
Kuerten S, Schickel A, Kerkloh C, Recks MS, Addicks K, Ruddle NH, Lehmann PV. Tertiary lymphoid organ development coincides with determinant spreading of the myelin-specific T cell response. Acta Neuropathologica 2012, 124: 861-873. PMID: 22842876, DOI: 10.1007/s00401-012-1023-3.Peer-Reviewed Original ResearchConceptsTertiary lymphoid organsExperimental autoimmune encephalomyelitisMyelin-specific T cell responseCentral nervous systemB cell aggregatesT cell responsesMultiple sclerosisB cell aggregationDeterminant spreadingB cellsCell responsesActive immune responseMyelin basic proteinLymphoid neogenesisAutoimmune encephalomyelitisMS patientsAggressive diseaseAutoimmune pathologyPatient populationLymphoid organsDisease onsetDisease progressionT cellsImmune responsePathogenic contribution
2009
Depletion of CD4+CD25+ T cells exacerbates experimental autoimmune encephalomyelitis induced by mouse, but not rat, antigens
Akirav EM, Bergman CM, Hill M, Ruddle NH. Depletion of CD4+CD25+ T cells exacerbates experimental autoimmune encephalomyelitis induced by mouse, but not rat, antigens. Journal Of Neuroscience Research 2009, 87: 3511-3519. PMID: 19125411, PMCID: PMC4429897, DOI: 10.1002/jnr.21981.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensAutoantigensAutoimmunityBiomarkersCD4 AntigensCD4-Positive T-LymphocytesCells, CulturedCentral Nervous SystemChemotaxis, LeukocyteDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleInterferon-gammaInterleukin-10Interleukin-17Interleukin-2 Receptor alpha SubunitLymphocyte ActivationMiceMice, Inbred C57BLMultiple SclerosisMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinRatsT-Lymphocytes, RegulatoryConceptsExperimental autoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinAutoimmune encephalomyelitisT cellsIL-10-producing cellsRegulatory T cellsTissue-restricted antigensCentral nervous systemField of autoimmunityT cell activationTreg depletionEAE severitySelf antigensOligodendrocyte glycoproteinForeign antigensExperimental diseaseNervous systemRelated antigensMiceSelf-antigen specificityAntigenTregsEncephalomyelitisAutoimmunityRats
2002
Altered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1–deficient mice
Graesser D, Solowiej A, Bruckner M, Osterweil E, Juedes A, Davis S, Ruddle NH, Engelhardt B, Madri JA. Altered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1–deficient mice. Journal Of Clinical Investigation 2002, 109: 383-392. PMID: 11827998, PMCID: PMC150854, DOI: 10.1172/jci13595.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisPECAM-1-deficient miceEndothelial cellsAutoimmune encephalomyelitisVascular permeabilityDevelopment of EAET lymphocyte transendothelial migrationEarly onsetHuman autoimmune disease multiple sclerosisAutoimmune disease multiple sclerosisCell adhesion molecule-1Altered vascular permeabilityCNS vascular permeabilityMononuclear cell extravasationDisease multiple sclerosisPlatelet/endothelial cell adhesion molecule-1Wild-type miceAdhesion molecule-1Endothelial cell adhesion molecule-1Subsets of leukocytesPECAM-1 expressionLymphocyte transendothelial migrationEarly time pointsHistamine challengeMultiple sclerosis
2000
Kinetics and Cellular Origin of Cytokines in the Central Nervous System: Insight into Mechanisms of Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis
Juedes A, Hjelmström P, Bergman C, Neild A, Ruddle N. Kinetics and Cellular Origin of Cytokines in the Central Nervous System: Insight into Mechanisms of Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis. The Journal Of Immunology 2000, 164: 419-426. PMID: 10605038, DOI: 10.4049/jimmunol.164.1.419.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCentral Nervous SystemChemokinesCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunophenotypingInflammation MediatorsInjections, SubcutaneousInterferon-gammaKineticsLymphocyte ActivationMacrophagesMiceMice, Inbred C57BLMicrogliaMolecular Sequence DataMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinSpleenTh1 CellsTh2 CellsTumor Necrosis Factor-alphaConceptsMyelin oligodendrocyte glycoproteinExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisOligodendrocyte glycoproteinTNF-alphaT cellsDay 7IFN-inducible protein-10TNF-alpha-producing cellsMonocyte chemotactic protein-1MOG35-55 peptideChronic clinical courseAnti-inflammatory cytokinesCD4 T cellsCourse of diseaseChemotactic protein-1Sensitive single-cell assayCellular originTNF-alpha productionRecruitment of macrophagesCentral nervous systemMOG35-55Clinical courseTh1 cytokinesTh2 cytokines