2016
Dendritic cells maintain dermal adipose–derived stromal cells in skin fibrosis
Chia JJ, Zhu T, Chyou S, Dasoveanu DC, Carballo C, Tian S, Magro CM, Rodeo S, Spiera RF, Ruddle NH, McGraw TE, Browning JL, Lafyatis R, Gordon JK, Lu TT. Dendritic cells maintain dermal adipose–derived stromal cells in skin fibrosis. Journal Of Clinical Investigation 2016, 126: 4331-4345. PMID: 27721238, PMCID: PMC5096920, DOI: 10.1172/jci85740.Peer-Reviewed Original ResearchConceptsAdipose-derived mesenchymal stromal cellsDendritic cellsSkin fibrosisDermal white adipose tissueFibrotic skinAdipose tissueStromal cellsMesenchymal stromal cell therapyScleroderma skin fibrosisStromal cell therapyWhite adipose tissueAdipose-derived stromal cellsMesenchymal stromal cellsΒ expressionMurine modelEffective treatmentFibrosisΒ1-integrin pathwayReparative functionsCell therapySclerodermaSkin functionIntegrin pathwaySurvivalAtrophy
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
A Switch in Pathogenic Mechanism in Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis in IFN-γ–Inducible Lysosomal Thiol Reductase-Free Mice
Bergman CM, Marta CB, Maric M, Pfeiffer SE, Cresswell P, Ruddle NH. A Switch in Pathogenic Mechanism in Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis in IFN-γ–Inducible Lysosomal Thiol Reductase-Free Mice. The Journal Of Immunology 2012, 188: 6001-6009. PMID: 22586035, PMCID: PMC4133136, DOI: 10.4049/jimmunol.1101898.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntigen-Presenting CellsEncephalomyelitis, Autoimmune, ExperimentalFluorescent Antibody TechniqueGlycoproteinsHumansImmunoblottingMiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataMyelin ProteinsMyelin-Oligodendrocyte GlycoproteinOxidoreductasesOxidoreductases Acting on Sulfur Group DonorsPeptide FragmentsRatsSequence Homology, Amino Acid
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
2010
Lymphotoxin-alpha contributes to lymphangiogenesis
Mounzer RH, Svendsen OS, Baluk P, Bergman CM, Padera TP, Wiig H, Jain RK, McDonald DM, Ruddle NH. Lymphotoxin-alpha contributes to lymphangiogenesis. Blood 2010, 116: 2173-2182. PMID: 20566898, PMCID: PMC2951858, DOI: 10.1182/blood-2009-12-256065.Peer-Reviewed Original ResearchPrevention of Diabetes by FTY720-Mediated Stabilization of Peri-Islet Tertiary Lymphoid Organs
Penaranda C, Tang Q, Ruddle NH, Bluestone JA. Prevention of Diabetes by FTY720-Mediated Stabilization of Peri-Islet Tertiary Lymphoid Organs. Diabetes 2010, 59: 1461-1468. PMID: 20299465, PMCID: PMC2874707, DOI: 10.2337/db09-1129.Peer-Reviewed Original ResearchConceptsTertiary lymphoid organsPancreatic lymph nodesNOD miceLymph nodesDiabetes developmentDiabetic miceLymphoid organsSpontaneous type 1 diabetesB cell compartmentalizationExit of lymphocytesNonobese diabetic (NOD) miceAge-matched miceDevelopment of diabetesPrevention of diabetesNaive T cellsType 1 diabetesB cell compartmentWeeks of ageSignificant insulitisIslet destructionTreatment withdrawalAutoimmune destructionClinical scoresAccelerated diseaseDisease progression
2006
Interaction of mature CD3+CD4+ T cells with dendritic cells triggers the development of tertiary lymphoid structures in the thyroid
Marinkovic T, Garin A, Yokota Y, Fu YX, Ruddle NH, Furtado GC, Lira SA. Interaction of mature CD3+CD4+ T cells with dendritic cells triggers the development of tertiary lymphoid structures in the thyroid. Journal Of Clinical Investigation 2006, 116: 2622-2632. PMID: 16998590, PMCID: PMC1570377, DOI: 10.1172/jci28993.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsB-LymphocytesCD3 ComplexCD4-Positive T-LymphocytesCell Adhesion MoleculesCell CommunicationCell MovementChemokine CCL21ChemokinesChemokines, CCDendritic CellsDNA-Binding ProteinsGene ExpressionGreen Fluorescent ProteinsInhibitor of Differentiation Protein 2Lymphoid TissueLymphotoxin-alphaMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicReceptors, CCR7Receptors, ChemokineThyroid DiseasesThyroid GlandSynchrony 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 KeywordsAnimalsBiomarkersB-LymphocytesCell Adhesion MoleculesCell CommunicationCells, CulturedDendritic CellsDown-RegulationEndotheliumImmunizationLymphangiogenesisLymphatic VesselsLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutMucoproteinsOxazolonePhenotypeReceptors, Tumor Necrosis FactorTime FactorsT-LymphocytesVenulesConceptsHigh 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
2005
Lymphotoxin Plays a Crucial Role in the Development and Function of Nasal-Associated Lymphoid Tissue through Regulation of Chemokines and Peripheral Node Addressin
Ying X, Chan K, Shenoy P, Hill M, Ruddle NH. Lymphotoxin Plays a Crucial Role in the Development and Function of Nasal-Associated Lymphoid Tissue through Regulation of Chemokines and Peripheral Node Addressin. American Journal Of Pathology 2005, 166: 135-146. PMID: 15632007, PMCID: PMC1602284, DOI: 10.1016/s0002-9440(10)62239-0.Peer-Reviewed Original ResearchConceptsHigh endothelial venulesLymphoid chemokinesIntranasal immunizationNasal-Associated Lymphoid TissueB cell compartmentalizationB cell zonesCervical lymph nodesSerum IgG titersLower cytokine levelsExpression of lymphotoxinImmediate postnatal periodRole of cytokinesRegulation of chemokinesWild-type miceGlyCAM-1Peripheral node addressinLymphoid tissue developmentNALT developmentSplenic cytokinesVaginal IgACytokine levelsLymph nodesIgG titersVascular addressinsLymphoid tissue
2004
IκB Kinase Complex α Kinase Activity Controls Chemokine and High Endothelial Venule Gene Expression in Lymph Nodes and Nasal-Associated Lymphoid Tissue
Drayton DL, Bonizzi G, Ying X, Liao S, Karin M, Ruddle NH. IκB Kinase Complex α Kinase Activity Controls Chemokine and High Endothelial Venule Gene Expression in Lymph Nodes and Nasal-Associated Lymphoid Tissue. The Journal Of Immunology 2004, 173: 6161-6168. PMID: 15528353, DOI: 10.4049/jimmunol.173.10.6161.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationChemokinesEndothelium, LymphaticEnzyme ActivationGene Expression Regulation, DevelopmentalI-kappa B KinaseLigandsLymph NodesLymphoid TissueLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsNasal MucosaProtein Serine-Threonine KinasesProtein SubunitsReceptors, Tumor Necrosis FactorConceptsHigh endothelial venulesSecondary lymphoid organogenesisLymph nodesAlternative NF-kappaB pathwayPeripheral node addressinNF-kappaB pathwayLymphoid tissueLymphoid organogenesisNasal-Associated Lymphoid TissueCell adhesion molecule-1Lymphoid chemokines CCL19Adhesion molecule-1GlyCAM-1Lymphotoxin beta receptorPathway activityNALT developmentChemokines CCL19Endothelial venulesBeta receptorsMolecule-1Mutant miceTarget genesCritical roleGene expressionReduced expressionMAdCAM-1 Expressing Sacral Lymph Node in the Lymphotoxin β-Deficient Mouse Provides a Site for Immune Generation Following Vaginal Herpes Simplex Virus-2 Infection
Soderberg KA, Linehan MM, Ruddle NH, Iwasaki A. MAdCAM-1 Expressing Sacral Lymph Node in the Lymphotoxin β-Deficient Mouse Provides a Site for Immune Generation Following Vaginal Herpes Simplex Virus-2 Infection. The Journal Of Immunology 2004, 173: 1908-1913. PMID: 15265924, DOI: 10.4049/jimmunol.173.3.1908.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, ViralCD4-Positive T-LymphocytesCell Adhesion MoleculesDendritic CellsFemaleHerpes GenitalisHerpesvirus 2, HumanImmunoglobulin GImmunoglobulinsLymph NodesLymphocyte ActivationLymphotoxin-alphaLymphotoxin-betaMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMucoproteinsSacrococcygeal RegionSplenectomyT-Cell Antigen Receptor SpecificityTh1 CellsVaginitisConceptsBeta-deficient miceSacral lymph nodesLymph nodesMesenteric lymph nodesWild-type miceGenital mucosaHerpes simplex virus 2 infectionIntravaginal HSV-2 infectionLT alpha-deficient miceMucosal addressin cell adhesion molecule-1Simplex virus 2 infectionCell adhesion molecule-1Mucosal lymph nodesAlpha-deficient miceCervical lymph nodesHSV-2 infectionVirus 2 infectionHSV type 2Potent immune responsesAdhesion molecule-1Intravaginal infectionTh1 responseDendritic cellsIgG responsesIliac artery
2002
Resident lung antigen-presenting cells have the capacity to promote Th2 T cell differentiation in situ
Constant SL, Brogdon JL, Piggott DA, Herrick CA, Visintin I, Ruddle NH, Bottomly K. Resident lung antigen-presenting cells have the capacity to promote Th2 T cell differentiation in situ. Journal Of Clinical Investigation 2002, 110: 1441-1448. PMID: 12438442, PMCID: PMC151814, DOI: 10.1172/jci16109.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntranasalAnimalsAntigen PresentationAntigen-Presenting CellsAntigens, ProtozoanCD4-Positive T-LymphocytesCell DifferentiationCell MovementCytokinesInterleukin-10Interleukin-6Leishmania majorLungLymph NodesLymphotoxin-alphaMiceMice, Inbred C57BLMice, KnockoutTh1 CellsTh2 CellsConceptsAntigen-presenting cellsTh2 T cell differentiationT cell primingT cell differentiationCell primingAntigen-loaded antigen-presenting cellsLung antigen-presenting cellsPulmonary antigen-presenting cellsResident antigen-presenting cellsPreferential primingAntigen-specific T cellsSecondary lymphoid organsTh2-dominated responsesTh1 responseAntigen exposureIL-10Th2 typeAntigen uptakeIL-6Lung microenvironmentLymphoid organsTh2 cellsIntranasal deliveryLung tissueAirway epitheliumAltered 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
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 productionInduction of oral tolerance to cellular immune responses in the absence of Peyer's patches
Spahn T, Fontana A, Faria A, Slavin A, Eugster H, Zhang X, Koni P, Ruddle N, Flavell R, Rennert P, Weiner H. Induction of oral tolerance to cellular immune responses in the absence of Peyer's patches. European Journal Of Immunology 2001, 31: 1278-1287. PMID: 11298355, DOI: 10.1002/1521-4141(200104)31:4<1278::aid-immu1278>3.0.co;2-a.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsAntibodiesDose-Response Relationship, ImmunologicEnzyme-Linked Immunosorbent AssayFecesGene DeletionHypersensitivity, DelayedImmune ToleranceImmunity, MucosalImmunoglobulin AInterferon-gammaInterleukin-2Lymph NodesLymphotoxin-alphaMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutOvalbuminPeyer's PatchesSignal TransductionTumor Necrosis Factor-alphaConceptsGut-associated lymphoid tissueMesenteric lymph nodesOral toleranceLow-dose oral toleranceDelayed-type hypersensitivity responseFecal IgA productionLTbeta-/- miceOral tolerance inductionLamina propria lymphocytesIntact immune systemCellular immune responsesPeripheral lymphoid organsIFN-gamma productionTumor necrosis factor familyProcessing of antigensNecrosis factor familySystemic hyporesponsivenessLymph nodesHypersensitivity responseTolerance inductionIgA productionIntraperitoneal administrationLymphoid organsLymphoid tissuePeyer's patchesLymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis
Goluszko E, Hjelmström P, Deng C, Poussin M, Ruddle N, Christadoss P. Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis. Journal Of Neuroimmunology 2001, 113: 109-118. PMID: 11137582, DOI: 10.1016/s0165-5728(00)00420-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAutoantibodiesB7-2 AntigenGene ExpressionImmunodominant EpitopesImmunoglobulin GImmunoglobulin MLymphotoxin-alphaMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMyasthenia Gravis, Autoimmune, ExperimentalReceptors, CholinergicReceptors, Tumor Necrosis FactorSpleenConceptsExperimental autoimmune myasthenia gravisClinical experimental autoimmune myasthenia gravisAutoimmune myasthenia gravisMyasthenia gravisMean titersPrimary humoral immune responseAlpha-deficient miceAnti-AChR antibodiesHumoral immune responseLower mean titersC57BL/6 miceImmunized miceTotal IgGDeficient miceIgG isotypeImmune responseAcetylcholine receptorsPartial preventionGravisMiceComplete preventionTitersLtPreventionPathogenesisICOS 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
1997
A Critical Role for Lymphotoxin in Experimental Allergic Encephalomyelitis
Suen W, Bergman C, Hjelmström P, Ruddle N. A Critical Role for Lymphotoxin in Experimental Allergic Encephalomyelitis. Journal Of Experimental Medicine 1997, 186: 1233-1240. PMID: 9334362, PMCID: PMC2199100, DOI: 10.1084/jem.186.8.1233.Peer-Reviewed Original ResearchConceptsExperimental allergic encephalomyelitisMaximum clinical scoreMyelin oligodendrocyte glycoproteinClinical scoresLT-alphaAllergic encephalomyelitisMultiple sclerosisCentral nervous system inflammationNervous system inflammationT cell productionDisease multiple sclerosisRat myelin oligodendrocyte glycoproteinAverage clinical scoreDisease indexWild-type littermatesWT T cellsNecrosis factor familyMOG 35CNS inflammationMOG antibodiesSystem inflammationWT miceC57BL/6 miceOligodendrocyte glycoproteinTNF-alphaDistinct Roles in Lymphoid Organogenesis for Lymphotoxins α and β Revealed in Lymphotoxin β–Deficient Mice
Koni P, Sacca R, Lawton P, Browning J, Ruddle N, Flavell R. Distinct Roles in Lymphoid Organogenesis for Lymphotoxins α and β Revealed in Lymphotoxin β–Deficient Mice. Immunity 1997, 6: 491-500. PMID: 9133428, DOI: 10.1016/s1074-7613(00)80292-7.Peer-Reviewed Original ResearchConceptsMesenteric lymph nodesLT alpha-deficient miceAlpha-deficient miceFollicular dendritic cellsBeta-deficient miceLymph nodesDendritic cellsDeficient miceLymphoid organogenesisTumor necrosis factor receptor type ILTbeta-deficient micePeripheral lymph nodesReceptor type ISplenic germinal centersLymphotoxin βPeyer's patchesGerminal centersLymphotoxin alphaLT-alphaLT alpha3Lymphotoxin αMiceUnidentified receptorType IAlpha