2016
The lymphotoxin β receptor is a potential therapeutic target in renal inflammation
Seleznik G, Seeger H, Bauer J, Fu K, Czerkowicz J, Papandile A, Poreci U, Rabah D, Ranger A, Cohen CD, Lindenmeyer M, Chen J, Edenhofer I, Anders HJ, Lech M, Wüthrich RP, Ruddle NH, Moeller MJ, Kozakowski N, Regele H, Browning JL, Heikenwalder M, Segerer S. The lymphotoxin β receptor is a potential therapeutic target in renal inflammation. Kidney International 2016, 89: 113-126. PMID: 26398497, DOI: 10.1038/ki.2015.280.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsCell LineChemokinesDisease Models, AnimalEpithelial CellsFemaleGlomerulonephritis, IGAHumansImmunoglobulinsKidney GlomerulusKidney TubulesLigandsLupus NephritisLymphocytesLymphotoxin beta ReceptorLymphotoxin-alphaLymphotoxin-betaMaleMesangial CellsMiceMiddle AgedRNA, MessengerSignal TransductionTranscriptomeConceptsTubular epithelial cellsParietal epithelial cellsEpithelial cellsRenal injuryLTβR signalingTherapeutic targetGlomerular immune complex depositionLymphotoxin β receptor (LTβR) signalingImproved renal functionSerum autoantibody titersHuman tubular epithelial cellsImmune complex depositionMurine lupus modelsProgressive kidney diseaseSuitable therapeutic targetPreclinical mouse modelsDifferent renal compartmentsPotential therapeutic targetΒ Receptor SignalingLymphotoxin β receptorAutoantibody titersRenal inflammationLupus modelsRenal functionRenal biopsy
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 expressionDetection of a Sulfotransferase (HEC-GlcNAc6ST) in High Endothelial Venules of Lymph Nodes and in High Endothelial Venule-Like Vessels within Ectopic Lymphoid Aggregates Relationship to the MECA-79 Epitope
Bistrup A, Tsay D, Shenoy P, Singer MS, Bangia N, Luther SA, Cyster JG, Ruddle NH, Rosen SD. Detection of a Sulfotransferase (HEC-GlcNAc6ST) in High Endothelial Venules of Lymph Nodes and in High Endothelial Venule-Like Vessels within Ectopic Lymphoid Aggregates Relationship to the MECA-79 Epitope. American Journal Of Pathology 2004, 164: 1635-1644. PMID: 15111310, PMCID: PMC1615668, DOI: 10.1016/s0002-9440(10)63722-4.Peer-Reviewed Original ResearchConceptsHigh endothelial venulesMECA-79 epitopeLymph nodesMECA-79Endothelial venulesHEC-GlcNAc6STHigh Endothelial Venule-Like VesselsLuminal stainingL-selectinMECA-79 monoclonal antibodyNull miceNonobese diabetic (NOD) miceHEV-like vesselsLymph nodes resultsHigh endothelial cellsLymphoid neogenesisDiabetic miceLymphocyte rollingLymphocyte homingMonoclonal antibodiesEndothelial cellsMiceConcomitant expressionEpitopesVenules
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 ResearchConceptsHigh 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