2020
CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses
Lin T, Geng T, Harrison AG, Yang D, Vella AT, Fikrig E, Wang P. CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses. Viruses 2020, 12: 1252. PMID: 33147869, PMCID: PMC7692144, DOI: 10.3390/v12111252.Peer-Reviewed Original ResearchConceptsChikungunya virusAlphaviral arthritisArthritogenic alphavirusesLargest immune cell populationMacrophages/T cellsImmune cell populationsInflammatory immune responseLow viral loadWild-type miceO'nyong-nyong virusWild-type animalsRheumatic manifestationsImmune infiltratesViral loadT cellsImmune responseAlphaviral diseaseArthritic diseasesTherapeutic targetCXCL10PathogenesisViral RNACell populationsArthritisFootpad
2016
Interleukin-17A Promotes CD8+ T Cell Cytotoxicity To Facilitate West Nile Virus Clearance
Acharya D, Wang P, Paul AM, Dai J, Gate D, Lowery JE, Stokic DS, Leis AA, Flavell RA, Town T, Fikrig E, Bai F. Interleukin-17A Promotes CD8+ T Cell Cytotoxicity To Facilitate West Nile Virus Clearance. Journal Of Virology 2016, 91: 10.1128/jvi.01529-16. PMID: 27795421, PMCID: PMC5165211, DOI: 10.1128/jvi.01529-16.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCytotoxicity, ImmunologicFemaleGene ExpressionHumansInterleukin-17MiceMice, Inbred C57BLNeuronsPrimary Cell CultureReceptors, Interleukin-17Recombinant ProteinsSurvival AnalysisT-Lymphocytes, CytotoxicTreatment OutcomeViral LoadVirus ReplicationWest Nile FeverWest Nile virusConceptsT cell cytotoxicityRecombinant IL-17AWest Nile virus infectionWNV-infected miceIL-17AT cellsViral burdenWNV infectionCell cytotoxicityInterleukin-17AVirus infectionMicrobial infectionsIL-17A-deficient miceT cell-mediated clearanceHigh viral burdenT-cell axisLethal WNV infectionSurvival of miceDay 6 postinfectionT cell functionWild-type miceDiverse immune functionsIL-17A.Proinflammatory cytokinesAutoimmune diseases
2012
Impaired Toll-Like Receptor 3-Mediated Immune Responses from Macrophages of Patients Chronically Infected with Hepatitis C Virus
Qian F, Bolen CR, Jing C, Wang X, Zheng W, Zhao H, Fikrig E, Bruce RD, Kleinstein SH, Montgomery RR. Impaired Toll-Like Receptor 3-Mediated Immune Responses from Macrophages of Patients Chronically Infected with Hepatitis C Virus. MSphere 2012, 20: 146-155. PMID: 23220997, PMCID: PMC3571267, DOI: 10.1128/cvi.00530-12.Peer-Reviewed Original ResearchMeSH KeywordsAdultFemaleGene ExpressionGenotypeHepacivirusHepatitis C, ChronicHumansInflammationInterferon-betaInterferonsInterleukinsLeukocytes, MononuclearMacrophagesMalePhosphorylationPolymorphism, Single NucleotideSignal TransductionSTAT1 Transcription FactorToll-Like Receptor 3Tumor Necrosis Factor-alphaViral LoadConceptsToll-like receptor 3Peripheral blood mononuclear cellsHepatitis C virusImmune responseHCV patientsC virusExpression of TLR3Clearance of HCVCommon chronic blood-borne infectionElevated innate immune responseImpaired toll-like receptorPrimary macrophagesHCV genotype 1Ongoing inflammatory responseMajority of patientsBlood-borne infectionsBlood mononuclear cellsToll-like receptorsIFN response genesPotential therapeutic approachInnate immune responseMacrophages of patientsElevated baseline expressionTLR3 pathwayViral clearance
2007
Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasion
Arjona A, Foellmer HG, Town T, Leng L, McDonald C, Wang T, Wong SJ, Montgomery RR, Fikrig E, Bucala R. Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasion. Journal Of Clinical Investigation 2007, 117: 3059-3066. PMID: 17909632, PMCID: PMC1994625, DOI: 10.1172/jci32218.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorMigration inhibitory factorViral neuroinvasionWest Nile virusInvolvement of MIFInhibitory factorProinflammatory cytokine macrophage migration inhibitory factorCytokine macrophage migration inhibitory factorWNV-infected miceBlood-brain barrierLife-threatening encephalitisWild-type miceAcute WNV infectionFlavivirus West Nile virusMIF expressionMIF levelsViral loadWNV encephalitisMIF actionPharmacotherapeutic approachesInflammatory responseWNV infectionCerebrospinal fluidSusceptible individualsInnate immunity
2005
Use of RNA Interference to Prevent Lethal Murine West Nile Virus Infection
Bai F, Wang T, Pal U, Bao F, Gould LH, Fikrig E. Use of RNA Interference to Prevent Lethal Murine West Nile Virus Infection. The Journal Of Infectious Diseases 2005, 191: 1148-1154. PMID: 15747251, DOI: 10.1086/428507.Peer-Reviewed Original ResearchConceptsWest Nile virusNile virusWest Nile virus infectionWest Nile virus replicationInjection 24 hAdministration of siRNAsIntraperitoneal inoculumViral loadProphylactic useFatal encephalitisLethal infectionVirus infectionViral infectionVirus replicationPartial protectionInfectionVirusMicePresent studyRNA interferenceEncephalitisSiRNAsAdministration
2004
Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis
Wang T, Town T, Alexopoulou L, Anderson JF, Fikrig E, Flavell RA. Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis. Nature Medicine 2004, 10: 1366-1373. PMID: 15558055, DOI: 10.1038/nm1140.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBlood-Brain BarrierBrainEncephalitisImmunohistochemistryInflammationMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMicroscopy, FluorescencePermeabilityReceptors, Cell SurfaceSignal TransductionToll-Like Receptor 3Toll-Like ReceptorsTumor Necrosis Factor-alphaViral LoadWest Nile virusConceptsToll-like receptor 3West Nile virusWNV infectionViral loadInflammatory responseReceptor 3Blood-brain barrier compromiseTLR3-deficient miceWest Nile virus entryLethal WNV infectionBlood-brain barrierWild-type miceNeuronal injuryIntracerebroventricular administrationBrain infectionCytokine productionBrain penetrationTumor necrosisTLR3 stimulationLethal encephalitisBarrier compromiseVariable severityInfectionVirus entryNile virus
2003
IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection
Wang T, Scully E, Yin Z, Kim JH, Wang S, Yan J, Mamula M, Anderson JF, Craft J, Fikrig E. IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection. The Journal Of Immunology 2003, 171: 2524-2531. PMID: 12928402, DOI: 10.4049/jimmunol.171.5.2524.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsBloodCell DivisionCells, CulturedCytotoxicity, ImmunologicEncephalitis, ViralFemaleGenes, T-Cell Receptor betaGenes, T-Cell Receptor deltaGenetic Predisposition to DiseaseInterferon-gammaLymphoid TissueMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaSeverity of Illness IndexT-Lymphocyte SubsetsViral LoadWest Nile FeverWest Nile virusConceptsGammadelta T cellsWN virus infectionT cellsVirus infectionIFN-gamma-producing gammadelta T cellsWest Nile virus infectionPrevention of mortalityΓδ T cellsSplenic T cellsWild-type miceEx vivo assaysAdoptive transferWest Nile virusPerforin expressionViral loadFatal meningoencephalitisIFN-gammaMiceInfectionWN virusNile virusVivo assaysLaboratory miceCellsVirus