2015
A Dendritic-Cell-Stromal Axis Maintains Immune Responses in Lymph Nodes
Kumar V, Dasoveanu DC, Chyou S, Tzeng TC, Rozo C, Liang Y, Stohl W, Fu YX, Ruddle NH, Lu TT. A Dendritic-Cell-Stromal Axis Maintains Immune Responses in Lymph Nodes. Immunity 2015, 42: 719-730. PMID: 25902483, PMCID: PMC4591553, DOI: 10.1016/j.immuni.2015.03.015.Peer-Reviewed Original ResearchConceptsDendritic cellsImmune responseReticular cellsLymph nodesFunction of DCsOngoing immune responseCell survivalSecondary lymphoid tissuesBeta-receptor ligandsStromal reticular cellsPathogenic lymphocytesLymphoproliferative diseaseLymphocyte functionLymphoid tissueLymphocyte survivalCritical mediatorPodoplaninReceptor ligandsCell functionSurvivalLTβRDiseasePotential strategyCellsResponse
2001
Lymphotoxin-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 preventionTitersLtPreventionPathogenesis
1996
Disruption of CD40–CD40 Ligand Interactions Results in an Enhanced Susceptibility to Leishmania amazonensis Infection
Soong L, Xu J, Grewal I, Kima P, Sun J, Longley B, Ruddle N, McMahon-Pratt D, Flavell R. Disruption of CD40–CD40 Ligand Interactions Results in an Enhanced Susceptibility to Leishmania amazonensis Infection. Immunity 1996, 4: 263-273. PMID: 8624816, DOI: 10.1016/s1074-7613(00)80434-3.Peer-Reviewed Original ResearchConceptsCD40L-/- miceImmune responseCD40-CD40 ligand interactionCD40L knockout miceLeishmania amazonensis infectionProgressive ulcerative lesionTissue parasite burdenCD40-CD40L interactionCellular immune responsesProtective immune responseWild-type miceHost immune responseImpaired T cellNitric oxide productionAmazonensis infectionUlcerative lesionsInflammatory responseNecrosis factorCD40 ligandT cellsIFN-gammaKnockout miceMacrophage activationParasite burdenOxide production