2022
APOBEC3A regulates transcription from interferon-stimulated response elements
Taura M, Frank JA, Takahashi T, Kong Y, Kudo E, Song E, Tokuyama M, Iwasaki A. APOBEC3A regulates transcription from interferon-stimulated response elements. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2011665119. PMID: 35549556, PMCID: PMC9171812, DOI: 10.1073/pnas.2011665119.Peer-Reviewed Original ResearchConceptsGene expressionResponse elementHost genomic lociInterferon-stimulated response elementRNA sequence analysisLong terminal repeatNegative feedback loopGenomic lociHuman genomeLethal mutationsProximal promoterHIV-1 transcriptionUnexpected roleIFN-I treatmentTerminal repeatDependent inductionViral genomeCytidine deaminaseISG15 inductionAntiviral responseA3AGenomeISG15 expressionType I IFNTranscription
2017
Type I IFN Is Necessary and Sufficient for Inflammation-Induced Red Blood Cell Alloimmunization in Mice
Gibb DR, Liu J, Natarajan P, Santhanakrishnan M, Madrid DJ, Eisenbarth SC, Zimring JC, Iwasaki A, Hendrickson JE. Type I IFN Is Necessary and Sufficient for Inflammation-Induced Red Blood Cell Alloimmunization in Mice. The Journal Of Immunology 2017, 199: 1041-1050. PMID: 28630094, PMCID: PMC5568771, DOI: 10.4049/jimmunol.1700401.Peer-Reviewed Original ResearchConceptsRBC alloimmunizationRed blood cell alloimmunizationCertain inflammatory disordersCompatible blood productsProduction of alloantibodiesHemolytic transfusion reactionsCytosolic pattern recognition receptorsType I IFNsTransgenic murine modelType I IFNPattern recognition receptorsTransfusion protocolAlloimmune responseRBC transfusionInflammatory disordersInflammatory conditionsTransfusion reactionsBlood productsInflammatory stimuliMurine modelI IFNsAlloimmunizationI IFNViral infectionRecognition receptors
2015
Toll-like receptor 9 trafficking and signaling for type I interferons requires PIKfyve activity
Hayashi K, Sasai M, Iwasaki A. Toll-like receptor 9 trafficking and signaling for type I interferons requires PIKfyve activity. International Immunology 2015, 27: 435-445. PMID: 25925170, PMCID: PMC4560039, DOI: 10.1093/intimm/dxv021.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineCell MembraneDendritic CellsDNA-Binding ProteinsEndosomesInterferon Type ILysosome-Associated Membrane GlycoproteinsMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProtein TransportSignal TransductionToll-Like Receptor 7Toll-Like Receptor 9Transcription FactorsVesicle-Associated Membrane Protein 3ConceptsDifferent dendritic cell subsetsIFN inductionDendritic cell subsetsInduction of cytokinesType I IFN inductionType I IFNType I interferonI IFN inductionViral nucleic acidsAnti-viral programsTLR9 traffickingCell subsetsTLR9 signalsI IFNI interferonInhibitor treatmentDistinct subcellular membranesRAW264.7 cellsType I interferon (IFN) genesTLR9Distinct endosomal compartmentsInterferon genesTLR traffickingConfocal microscopyInductionTemperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells
Foxman EF, Storer JA, Fitzgerald ME, Wasik BR, Hou L, Zhao H, Turner PE, Pyle AM, Iwasaki A. Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 827-832. PMID: 25561542, PMCID: PMC4311828, DOI: 10.1073/pnas.1411030112.Peer-Reviewed Original ResearchConceptsAirway cellsCommon cold virusViral replicationIFN inductionRecombinant type I IFNMouse airway epithelial cellsCold virusAirway epithelial cellsInduction of ISGsType I IFNPrimary airway cellsCore body temperatureType IAntiviral defense responseLike receptorsI IFNNasal cavityMAVS proteinHuman rhinovirusSustained increaseInnate defensePoly IGenetic deficiencyRobust inductionRhinovirus
2013
Innate immunity
Iwasaki A, Peiris M. Innate immunity. 2013, 267-282. DOI: 10.1002/9781118636817.ch17.Peer-Reviewed Original ResearchToll-like receptorsNOD-like receptorsImmune responseVirus infectionInfluenza virusHundreds of IFNProtective host responseInfluenza virus infectionAdaptive immune responsesInnate immune responseType I IFNInfluenza virus replicationInnate immune systemDendritic cellsNK cellsInfluenza infectionIL-1βInnate sensorsAdaptive immunityLike receptorsDetrimental pathologyI IFNAlveolar macrophagesHost responseImmune system
2010
CD8+ T Cell Responses following Replication-Defective Adenovirus Serotype 5 Immunization Are Dependent on CD11c+ Dendritic Cells but Show Redundancy in Their Requirement of TLR and Nucleotide-Binding Oligomerization Domain-Like Receptor Signaling
Lindsay RW, Darrah PA, Quinn KM, Wille-Reece U, Mattei LM, Iwasaki A, Kasturi SP, Pulendran B, Gall JG, Spies AG, Seder RA. CD8+ T Cell Responses following Replication-Defective Adenovirus Serotype 5 Immunization Are Dependent on CD11c+ Dendritic Cells but Show Redundancy in Their Requirement of TLR and Nucleotide-Binding Oligomerization Domain-Like Receptor Signaling. The Journal Of Immunology 2010, 185: 1513-1521. PMID: 20610651, DOI: 10.4049/jimmunol.1000338.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviruses, HumanAnimalsAntigen PresentationCD11c AntigenCD8-Positive T-LymphocytesDefective VirusesDendritic CellsImmunity, InnateImmunophenotypingInterferon Type IInterleukin-12Intracellular Signaling Peptides and ProteinsLymph NodesMiceMice, Inbred C57BLMice, KnockoutOligodeoxyribonucleotidesSignal TransductionToll-Like ReceptorsViral VaccinesVirionConceptsT cell responsesCD8 T cell responsesDendritic cellsCell responsesRAd5 immunizationCD8 responsesDC subsetsInnate cytokinesOligomerization domain-like receptor protein 3Domain-like receptor protein 3OT-I CD8 T cellsCD4 T cell responsesCD8 T cell proliferationNucleotide-Binding Oligomerization DomainReplication-defective adenovirus serotype 5Plasmacytoid dendritic cellsReceptor protein 3CD8 T cellsDistinct DC subsetsT cell immunityApoptosis-associated speck-like proteinPre-existing immunityT cell proliferationLike receptor signalingType I IFN
2009
Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling
Tal MC, Sasai M, Lee HK, Yordy B, Shadel GS, Iwasaki A. Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 2770-2775. PMID: 19196953, PMCID: PMC2650341, DOI: 10.1073/pnas.0807694106.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutophagyAutophagy-Related Protein 5Cells, CulturedDEAD Box Protein 58DEAD-box RNA HelicasesDNA, MitochondrialEnzyme-Linked Immunosorbent AssayFlow CytometryInterferon Type IMacrophagesMiceMicrotubule-Associated ProteinsMitochondriaReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionSignal TransductionConceptsReactive oxygen speciesDysfunctional mitochondriaInnate antiviral defenseAntiviral defenseKey antiviral cytokinesAbsence of autophagyMitochondrial reactive oxygen speciesHomeostatic regulationRole of autophagyTreatment of cellsIPS-1RLR signalingVesicular stomatitis virusAutophagy resultsRNA virusesWT cellsMitochondriaAutophagyType I IFNStomatitis virusRLRLike receptorsOxygen speciesNeurodegenerative diseasesInflammatory disorders
2006
Cutting Edge: Plasmacytoid Dendritic Cells Provide Innate Immune Protection against Mucosal Viral Infection In Situ
Lund JM, Linehan MM, Iijima N, Iwasaki A. Cutting Edge: Plasmacytoid Dendritic Cells Provide Innate Immune Protection against Mucosal Viral Infection In Situ. The Journal Of Immunology 2006, 177: 7510-7514. PMID: 17114418, DOI: 10.4049/jimmunol.177.11.7510.Peer-Reviewed Original ResearchConceptsMucosal viral infectionsPlasmacytoid dendritic cellsPlasmacytoid DCsDendritic cellsViral infectionGenital HSV-2 infectionHSV-2 infectionLocal viral replicationAntiviral effector cellsInnate immune protectionTLR9-dependent mannerType I IFNsType I IFNPeripheral mucosaPowerful APCsTh1 immunityEffector cellsImmune protectionNaive lymphocytesAdaptive immunityI IFNsI IFNVaginal mucosaViral replicationInnate defense