2022
CD55 Facilitates Immune Evasion by Borrelia crocidurae, an Agent of Relapsing Fever
Arora G, Lynn GE, Tang X, Rosen CE, Hoornstra D, Sajid A, Hovius JW, Palm NW, Ring AM, Fikrig E. CD55 Facilitates Immune Evasion by Borrelia crocidurae, an Agent of Relapsing Fever. MBio 2022, 13: e01161-22. PMID: 36036625, PMCID: PMC9600505, DOI: 10.1128/mbio.01161-22.Peer-Reviewed Original ResearchConceptsRole of CD55Fever infectionImmune evasionSurface of erythrocytesRosette formationB. crociduraeB. persicaHost factorsBorrelia crociduraeAcute febrile illnessInflammatory cytokine levelsElevated proinflammatory cytokinesExpression of CD55Causative agentErythrocyte rosette formationFacilitates Immune EvasionComplement-mediated lysisHost-pathogen interactionsCytokine levelsFebrile illnessSignificant morbidityProinflammatory cytokinesHigh-throughput screenC5a levelsCD55 expression
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
IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis
Wang P, Bai F, Zenewicz LA, Dai J, Gate D, Cheng G, Yang L, Qian F, Yuan X, Montgomery RR, Flavell RA, Town T, Fikrig E. IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis. PLOS ONE 2012, 7: e44153. PMID: 22952908, PMCID: PMC3429482, DOI: 10.1371/journal.pone.0044153.Peer-Reviewed Original ResearchConceptsWild-type miceCentral nervous systemIL-22Viral loadNeutrophil migrationType miceWest Nile virus encephalitisSimilar viral loadsLethal WNV infectionIL-22 signalingHost immune responseWNV neuroinvasionVirus encephalitisCXCR2 ligandsLeukocyte infiltrateProinflammatory cytokinesChemokine receptorsImmune responseWNV infectionViral infectionNervous systemSignaling contributesExtracellular pathogensNon-redundant roleWT leukocytes
2011
Circadian rhythms influence disease severity in a mouse model of sepsis (110.9)
Walker W, Bozzi A, Fikrig E. Circadian rhythms influence disease severity in a mouse model of sepsis (110.9). The Journal Of Immunology 2011, 186: 110.9-110.9. DOI: 10.4049/jimmunol.186.supp.110.9.Peer-Reviewed Original ResearchInflammatory responseMouse modelCircadian rhythmSerum proinflammatory cytokinesPuncture (CLP) mouse modelRisk of mortalitySeptic patientsSepsis inductionCecal ligationSepsis phenotypesEarly mortalityProinflammatory cytokinesSevere hypothermiaDisease scoreCLP modelDisease severitySepsisCreatine kinaseMortalityPatientsMiceRhythmSeverityTime 19Mammalian physiology
2009
Innate Immune Responses to West Nile Virus Infection
Arjona A, Fikrig E. Innate Immune Responses to West Nile Virus Infection. Emerging Infectious Diseases Of The 21st Century 2009, 169-187. DOI: 10.1007/978-0-387-79840-0_8.Peer-Reviewed Original ResearchWest Nile virus infectionPathogen recognition receptorsImmune cellsVirus infectionImmune responseBlood-brain barrier permeabilityInnate immune cellsAdaptive immune responsesInnate immune mechanismsInnate immune responseInnate antiviral immunityWNV neuroinvasionProinflammatory cytokinesCostimulatory moleculesImmune mechanismsBarrier permeabilityAntiviral immunityWNV infectionInnate responseAntiviral stateInfectionCytokinesDetrimental effectsCurrent understandingImmunopathogenesis
2008
West Nile Virus Attenuates Activation of Primary Human Macrophages
Kong KF, Wang X, Anderson JF, Fikrig E, Montgomery RR. West Nile Virus Attenuates Activation of Primary Human Macrophages. Viral Immunology 2008, 21: 78-82. PMID: 18355125, PMCID: PMC2666911, DOI: 10.1089/vim.2007.0072.Peer-Reviewed Original ResearchConceptsWest Nile virusPrimary human macrophagesHuman macrophagesWNV infectionProduction of interleukinMosquito-borne flavivirusType I interferonProinflammatory cytokinesPotent therapyJAK/STAT pathwayIL-1betaEffective treatmentMacrophage activationI interferonRelated flavivirusesInfectionAttenuate activationNile virusMacrophagesSTAT pathwayFlavivirusesActivationDifferential responseInterleukinCytokines
2007
West Nile Virus Envelope Protein Inhibits dsRNA-Induced Innate Immune Responses
Arjona A, Ledizet M, Anthony K, Bonafé N, Modis Y, Town T, Fikrig E. West Nile Virus Envelope Protein Inhibits dsRNA-Induced Innate Immune Responses. The Journal Of Immunology 2007, 179: 8403-8409. PMID: 18056386, DOI: 10.4049/jimmunol.179.12.8403.Peer-Reviewed Original ResearchConceptsWest Nile virusInnate immune responseReceptor-interacting protein 1Immune responseMajor structural proteinVirus-associated molecular patternsDipteran cellsViral replication intermediatesRNA helicasesAdaptor molecule TRIFReplication intermediatesStructural proteinsWNV envelope proteinGlycosylation patternsMolecular patternsAntiviral stateGlycosylation profileProtein 1Murine macrophagesProinflammatory cytokinesCytokine productionImmunosuppressive effectsDsRNAImmune cellsEnvelope protein
2002
Murine Lyme Arthritis Development Mediated by p38 Mitogen-Activated Protein Kinase Activity
Anguita J, Barthold SW, Persinski R, Hedrick MN, Huy CA, Davis RJ, Flavell RA, Fikrig E. Murine Lyme Arthritis Development Mediated by p38 Mitogen-Activated Protein Kinase Activity. The Journal Of Immunology 2002, 168: 6352-6357. PMID: 12055252, PMCID: PMC4309983, DOI: 10.4049/jimmunol.168.12.6352.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, BacterialArthritis, InfectiousBorrelia burgdorferiCD4-Positive T-LymphocytesCell LineEnzyme ActivationInflammationInterferon-gammaLyme DiseaseMAP Kinase Kinase 3MAP Kinase Signaling SystemMiceMice, KnockoutMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesP38 Mitogen-Activated Protein KinasesPhagocytesPhosphorylationProtein-Tyrosine KinasesReceptors, InterferonConceptsProinflammatory cytokine productionCytokine productionT helper type 1 responsePhagocytic cellsDevelopment of arthritisPotential new therapeutic approachType 1 responseInfection of miceExperimental murine modelMurine Lyme arthritisNew therapeutic approachesLyme arthritis developmentTreatment of inflammationCytokine burstArthritis developmentJoint inflammationLyme arthritisNF-kappa BProinflammatory cytokinesTNF-alphaT cellsMurine modelTherapeutic approachesP38 MAP kinaseSpecific Abs