2020
Basics of Inducible Lymphoid Organs
Ruddle NH. Basics of Inducible Lymphoid Organs. Current Topics In Microbiology And Immunology 2020, 426: 1-19. PMID: 32588229, DOI: 10.1007/82_2020_218.Peer-Reviewed Original ResearchConceptsTertiary lymphoid organsSecondary lymphoid organsLymphoid tissue organizerHigh endothelial venulesLymphoid organsDendritic cellsB cellsEctopic lymphoid organsFollicular dendritic cellsTertiary lymphoid structuresTertiary lymphoid tissueLymph nodesNK cellsChronic inflammationLTi cellsLymphoid structuresTolerance inductionInducer cellsLymphoid tissueEndothelial venulesAntigen presentationT cellsAccumulation of cellsStromal cellsAutoimmunity
2019
Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis
Camell CD, Günther P, Lee A, Goldberg EL, Spadaro O, Youm YH, Bartke A, Hubbard GB, Ikeno Y, Ruddle NH, Schultze J, Dixit VD. Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis. Cell Metabolism 2019, 30: 1024-1039.e6. PMID: 31735593, PMCID: PMC6944439, DOI: 10.1016/j.cmet.2019.10.006.Peer-Reviewed Original ResearchConceptsAge-associated B cellsFat-associated lymphoid clustersB cellsAdipose tissue leukocytesB-cell depletionB cell accumulationBody temperature maintenanceFALC formationVisceral adiposityCell depletionNLRP3 inflammasomeFemale miceLymphoid clustersMetabolic dysfunctionIL-1Metabolic impairmentIL-1RTissue leukocytesCell accumulationMetabolic homeostasisUnique populationLipolysisCellsTemperature maintenanceAdiposityAdaptive Immunity: Effector Functions, Regulation, and Vaccination
Kavathas P, Krause P, Ruddle N. Adaptive Immunity: Effector Functions, Regulation, and Vaccination. 2019, 75-95. DOI: 10.1007/978-3-030-25553-4_5.ChaptersAntigen-presenting cellsT cellsB cellsImmune responseInnate cellsEffector cellsInnate antigen-presenting cellsCD4 T helper cellsEffector T cellsB memory cellsT helper cellsSecondary lymphoid organsNaive T cellsBalanced immune responsePathogen-infected host cellsCD4 subsetCytokine milieuHelper cellsLymphoid organsEffector TPlasma cellsEffector functionsAdaptive immuneTypes of pathogensMacrophage responseOrganization and Cells of the Immune System
Kavathas P, Krause P, Ruddle N. Organization and Cells of the Immune System. 2019, 21-38. DOI: 10.1007/978-3-030-25553-4_2.ChaptersImmune cellsImmune systemLymphoid organsDifferent immune cell typesTertiary lymphoid organsInnate lymphoid cellsDifferent immune cellsSecondary lymphoid organsImmune cell typesLymphatic vesselsAdaptive immune systemHuman immune systemDendritic cellsBarrier immunityChronic inflammationUrinary tractSoluble mediatorsLymphoid cellsB cellsLymphoid systemMucosal surfacesChemokinesCytokinesOrgansCell types
2016
High Endothelial Venules and Lymphatic Vessels in Tertiary Lymphoid Organs: Characteristics, Functions, and Regulation
Ruddle NH. High Endothelial Venules and Lymphatic Vessels in Tertiary Lymphoid Organs: Characteristics, Functions, and Regulation. Frontiers In Immunology 2016, 7: 491. PMID: 27881983, PMCID: PMC5101196, DOI: 10.3389/fimmu.2016.00491.Peer-Reviewed Original ResearchTertiary lymphoid organsHigh endothelial venulesSecondary lymphoid organsLymph nodesAntigen-presenting cellsLymphoid organsEndothelial venulesLymphatic vesselsStromal cellsCentral memory cellsPrimary lymphoid organsTransport antigensGraft rejectionEffector cellsChemokine expressionChronic inflammationPeyer's patchesAntigen presentationInflammatory signalsB cellsBone marrowImmune systemReticular cellsMicrobial infectionsCellular composition
2013
Identification of a New Stromal Cell Type Involved in the Regulation of Inflamed B Cell Follicles
Mionnet C, Mondor I, Jorquera A, Loosveld M, Maurizio J, Arcangeli ML, Ruddle NH, Nowak J, Aurrand-Lions M, Luche H, Bajénoff M. Identification of a New Stromal Cell Type Involved in the Regulation of Inflamed B Cell Follicles. PLOS Biology 2013, 11: e1001672. PMID: 24130458, PMCID: PMC3794863, DOI: 10.1371/journal.pbio.1001672.Peer-Reviewed Original ResearchConceptsStromal cell typesB cell folliclesT cell zonesCell typesFate-mapping systemStromal cellsCellular demandB cellsLymph Node Stromal CellsSurvival signalsStromal cell subsetsB cell ablationLN stromal cellsCell zoneAdhesive substrataCell ablationCell subsetsImmune responseCellsFolliclesInflammationSubstrataRegulationTransient boundaryLymphocytes
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
2011
Blocking lymphotoxin signaling abrogates the development of ectopic lymphoid tissue within cardiac allografts and inhibits effector antibody responses
Motallebzadeh R, Rehakova S, Conlon TM, Win TS, Callaghan CJ, Goddard M, Bolton EM, Ruddle NH, Bradley JA, Pettigrew GJ. Blocking lymphotoxin signaling abrogates the development of ectopic lymphoid tissue within cardiac allografts and inhibits effector antibody responses. The FASEB Journal 2011, 26: 51-62. PMID: 21926237, DOI: 10.1096/fj.11-186973.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesBone MarrowCD4-Positive T-LymphocytesChoristomaChronic DiseaseGraft RejectionHeart TransplantationIsoantibodiesLymphoid TissueLymphotoxin beta ReceptorLymphotoxin-betaMiceMice, Inbred C57BLMice, KnockoutMyocardiumNeovascularization, PathologicRecombinant Fusion ProteinsSignal TransductionSpleenTransplantation, HomologousConceptsTertiary lymphoid organsCardiac allograftsHeart allograftsB cellsLymphotoxin β receptor (LTβR) signalingEctopic lymphoid tissueGerminal center activityLTβR-IgTLO formationPostoperative administrationAccelerated rejectionHumoral autoimmunityAlloimmune responseAutoantibody productionAutoantibody responseHumoral responseLymphoid organsLymphoid tissueLymphoid organogenesisEffector antibodiesMouse modelAllograftsTransplantationAutoantibodiesCellsResident B cells regulate thymic expression of myelin oligodendrocyte glycoprotein
Akirav EM, Xu Y, Ruddle NH. Resident B cells regulate thymic expression of myelin oligodendrocyte glycoprotein. Journal Of Neuroimmunology 2011, 235: 33-39. PMID: 21550671, PMCID: PMC3157307, DOI: 10.1016/j.jneuroim.2011.03.013.Peer-Reviewed Original ResearchConceptsB cellsB cell-deficient μMT miceMyelin oligodendrocyte glycoproteinResident B cellsThymic B cellsCortico-medullary junctionMinor cell populationProduction of LTInsulin mRNA expressionΜMT miceEpithelial cell numberOligodendrocyte glycoproteinThymic expressionAntigen expressionMRNA expressionNormal tissuesCell populationsCell numberCellsExpressionLtUnexpected roleBiological roleLymphotoxinMice
2006
Synchrony of High Endothelial Venules and Lymphatic Vessels Revealed by Immunization
Liao S, Ruddle NH. Synchrony of High Endothelial Venules and Lymphatic Vessels Revealed by Immunization. The Journal Of Immunology 2006, 177: 3369-3379. PMID: 16920978, DOI: 10.4049/jimmunol.177.5.3369.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesBiomarkersCell Adhesion MoleculesCell CommunicationCells, CulturedDendritic CellsDown-RegulationEndotheliumImmunizationLymphangiogenesisLymphatic VesselsLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutMucoproteinsOxazolonePhenotypeReceptors, Tumor Necrosis FactorT-LymphocytesTime FactorsVenulesConceptsHigh endothelial venulesB cellsEndothelial venulesPLN high endothelial venulesPeripheral lymph node high endothelial venulesLymph node high endothelial venulesMature phenotypeLTbetaR-Ig treatmentT cell primingLYVE-1Evans blue dyeLymphotoxin beta receptorLTbetaR-IgCell primingLV functionOVA immunizationImmature phenotypeDay 7Day 4Functional insufficiencyImmunizationClose physical contactLVRemodeling processLymphatic vessels
2003
Rat and Human Myelin Oligodendrocyte Glycoproteins Induce Experimental Autoimmune Encephalomyelitis by Different Mechanisms in C57BL/6 Mice
Oliver AR, Lyon GM, Ruddle NH. Rat and Human Myelin Oligodendrocyte Glycoproteins Induce Experimental Autoimmune Encephalomyelitis by Different Mechanisms in C57BL/6 Mice. The Journal Of Immunology 2003, 171: 462-468. PMID: 12817031, DOI: 10.4049/jimmunol.171.1.462.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntigen PresentationAutoantibodiesB-LymphocytesCell MovementDose-Response Relationship, ImmunologicEncephalomyelitis, Autoimmune, ExperimentalFemaleGlycoproteinsHumansImmunoglobulin GInjections, IntramuscularInterferon-gammaInterleukin-13MiceMice, Inbred C57BLMice, Mutant StrainsMolecular Sequence DataMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsRatsSpecies SpecificitySpinal CordConceptsExperimental autoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinRat myelin oligodendrocyte glycoproteinHuman myelin oligodendrocyte glycoproteinMOG 35C57BL/6 miceMOG proteinAutoimmune encephalomyelitisOligodendrocyte glycoproteinB cellsCell responsesEncephalitogenic T cell responsesB cell-deficient miceB cell dependenceCell-deficient miceT cell responsesB cell responsesDifferent pathogenic mechanismsCNS infiltratesIL-13T cellsSpleen cellsIFN-gammaIgG subclassesAg presentationHelicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue
Shomer NH, Fox JG, Juedes AE, Ruddle NH. Helicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue. Infection And Immunity 2003, 71: 3572-3577. PMID: 12761142, PMCID: PMC155770, DOI: 10.1128/iai.71.6.3572-3577.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationAntigens, SurfaceAutoimmunityCell Adhesion MoleculesCell AggregationChemokine CCL21Chemokine CXCL13Chemokines, CCChemokines, CXCHelicobacter InfectionsHepatitis, ChronicImmunoglobulinsLiverLymphoid TissueMembrane ProteinsMiceMucoproteinsVascular Cell Adhesion Molecule-1ConceptsChronic active hepatitisTertiary lymphoid organsLymphoid organsActive hepatitisInflammatory lesionsHepatic inflammatory lesionsMucosal addressin cell adhesion moleculeTertiary lymphoid tissuePeripheral node addressinLiver cell suspensionsLiver tissue sectionsB220-positive B cellsChemokines SLCHepatic inflammationInflammatory infiltrateChronic autoimmunityLymphoid aggregatesLymphoid tissueFluorescence-activated cell sortingT cellsCell adhesion moleculeB cellsStromal cellsSmall venulesAdhesion molecules
2001
ICOS co-stimulatory receptor is essential for T-cell activation and function
Dong C, Juedes A, Temann U, Shresta S, Allison J, Ruddle N, Flavell R. ICOS co-stimulatory receptor is essential for T-cell activation and function. Nature 2001, 409: 97-101. PMID: 11343121, DOI: 10.1038/35051100.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntibody FormationAntigens, CDAntigens, Differentiation, T-LymphocyteCell DifferentiationCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalGene TargetingHemocyaninsInducible T-Cell Co-Stimulator ProteinInterleukin-13Interleukin-4Lymph NodesLymphocyte ActivationMiceMice, KnockoutMolecular Sequence DataMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinT-LymphocytesConceptsInducible co-stimulatory moleculeT cell activationCo-stimulatory moleculesT cellsICOS-/- miceICOS-deficient miceInflammatory autoimmune diseaseExperimental autoimmune encephalomyelitisInjection of lipopolysaccharideCo-stimulatory receptorsHumoral immune responseNon-immune tissuesT lymphocyte activationAutoimmune encephalomyelitisAutoimmune diseasesImmune responseInterleukin-4Immune functionCD28/CTLA4 familyB cellsProtective roleEnhanced susceptibilityActivationReceptorsHigh affinity
2000
Lymphotoxin in inflammation and lymphoid organ development: Variations on a theme
Ruddle N. Lymphotoxin in inflammation and lymphoid organ development: Variations on a theme. Progress In Inflammation Research 2000, 83-88. DOI: 10.1007/978-3-0348-8468-6_8.Peer-Reviewed Original ResearchAutoimmune diseasesLymphoid organsLymphoid organ developmentT cellsTarget organsAntigen-specific T cellsAdditional T cellsLocal lymphoid organsTertiary lymphoid organsConsequence of inflammationLymphoid neogenesisClinical relapseAutoimmune inflammationLocal target organLymphoid tissueInflammatory reactionB cellsInflammationTransgenic miceTissue damageDiseaseTNF familyOrgansUnrelated moleculesOrgan development
1993
Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice.
Picarella DE, Kratz A, Li CB, Ruddle NH, Flavell RA. Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. The Journal Of Immunology 1993, 150: 4136-50. PMID: 7682590, DOI: 10.4049/jimmunol.150.9.4136.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, SurfaceCD4 AntigensCD8 AntigensCell Adhesion MoleculesDiabetes Mellitus, Type 1Histocompatibility Antigens Class IIHumansIntercellular Adhesion Molecule-1Islets of LangerhansKidneyLeukocyte Common AntigensLymphotoxin-alphaMiceMice, Inbred NODMice, TransgenicPancreatitisProtein Tyrosine Phosphatase, Non-Receptor Type 1Receptors, Interleukin-2Tumor Necrosis Factor-alphaUp-RegulationConceptsTNF-alphaTransgenic miceTNF-alpha transgenic miceInsulin-dependent diabetes mellitusAdhesion molecules VCAM-1Rat insulin II promoterTNF-alpha transgeneRole of TNFMurine TNF-alphaTumor necrosis factorRegulation of inflammationMHC class IReduced insulin contentPeri-insulitisIslet destructionDiabetes mellitusAutoimmune diseasesAlpha productionIslet endotheliumNecrosis factorT cellsICAM-1VCAM-1Insulin contentB cells
1992
Insulitis in transgenic mice expressing tumor necrosis factor beta (lymphotoxin) in the pancreas.
Picarella DE, Kratz A, Li CB, Ruddle NH, Flavell RA. Insulitis in transgenic mice expressing tumor necrosis factor beta (lymphotoxin) in the pancreas. Proceedings Of The National Academy Of Sciences Of The United States Of America 1992, 89: 10036-10040. PMID: 1279667, PMCID: PMC50272, DOI: 10.1073/pnas.89.21.10036.Peer-Reviewed Original ResearchConceptsNecrosis factor betaTransgenic miceFactor betaInsulin-dependent diabetes mellitusRat insulin II promoterTumor necrosis factor betaType 1 diabetesRegulation of inflammationTNF-beta geneDiabetes mellitusInflammatory infiltrateInflammatory diseasesT cellsImmune responseB cellsInsulitisDiabetesMicePancreasImportant early stepBetaEarly stagesCD8InfiltratesMellitus