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
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
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
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
Altered 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
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