2014
Pillars article: Abnormal development of peripheral lymphoid organs in mice deficient in lymphotoxin. Science. 1994. 264: 703-707.
De Togni P, Goellner J, Ruddle NH, Streeter PR, Andrea F, Mariathasan S, Smith SC, Carlson R, Shornick LP, Strauss-Schoenberger J, Russell JH, Karr R, Chaplin DD. Pillars article: Abnormal development of peripheral lymphoid organs in mice deficient in lymphotoxin. Science. 1994. 264: 703-707. The Journal Of Immunology 2014, 192: 2010-4. PMID: 24563504.Peer-Reviewed Original Research
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 expression
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 presentation
2001
Sulfation of L-Selectin Ligands by an HEV-Restricted Sulfotransferase Regulates Lymphocyte Homing to Lymph Nodes
Hemmerich S, Bistrup A, Singer M, van Zante A, Lee J, Tsay D, Peters M, Carminati J, Brennan T, Carver-Moore K, Leviten M, Fuentes M, Ruddle N, Rosen S. Sulfation of L-Selectin Ligands by an HEV-Restricted Sulfotransferase Regulates Lymphocyte Homing to Lymph Nodes. Immunity 2001, 15: 237-247. PMID: 11520459, DOI: 10.1016/s1074-7613(01)00188-1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell AdhesionChemotaxis, LeukocyteLectinsLigandsL-SelectinLymph NodesLymphatic SystemLymphocytesMiceMice, Mutant StrainsSulfotransferasesConceptsHigh endothelial venulesLymph nodesL-selectinLuminal aspectChronic inflammatory sitesHEC-GlcNAc6STImportant therapeutic targetL-selectin ligandsMECA-79Lymphocyte traffickingEndothelial venulesInflammatory sitesTherapeutic targetLymphocyte homingLymphocyte bindingGenetic deletionSpecific ligandsLigand activityRecombinant L-selectinSulfotransferaseCritical roleEssential posttranslational modificationVenules
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