2021
KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements
Zhang SM, Cai WL, Liu X, Thakral D, Luo J, Chan LH, McGeary MK, Song E, Blenman KRM, Micevic G, Jessel S, Zhang Y, Yin M, Booth CJ, Jilaveanu LB, Damsky W, Sznol M, Kluger HM, Iwasaki A, Bosenberg MW, Yan Q. KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements. Nature 2021, 598: 682-687. PMID: 34671158, PMCID: PMC8555464, DOI: 10.1038/s41586-021-03994-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorDNA-Binding ProteinsEpigenesis, GeneticGene SilencingHeterochromatinHistone-Lysine N-MethyltransferaseHumansInterferon Type IJumonji Domain-Containing Histone DemethylasesMaleMelanomaMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsRepressor ProteinsRetroelementsTumor EscapeConceptsImmune checkpoint blockadeImmune evasionCheckpoint blockadeImmune responseAnti-tumor immune responseRobust adaptive immune responseTumor immune evasionAnti-tumor immunityAdaptive immune responsesType I interferon responseDNA-sensing pathwayMouse melanoma modelImmunotherapy resistanceMost patientsCurrent immunotherapiesTumor immunogenicityImmune memoryMelanoma modelCytosolic RNA sensingRole of KDM5BConsiderable efficacyInterferon responseImmunotherapyEpigenetic therapyBlockade
2019
Aedes aegypti AgBR1 antibodies modulate early Zika virus infection of mice
Uraki R, Hastings AK, Marin-Lopez A, Sumida T, Takahashi T, Grover JR, Iwasaki A, Hafler DA, Montgomery RR, Fikrig E. Aedes aegypti AgBR1 antibodies modulate early Zika virus infection of mice. Nature Microbiology 2019, 4: 948-955. PMID: 30858571, PMCID: PMC6533137, DOI: 10.1038/s41564-019-0385-x.Peer-Reviewed Original ResearchConceptsZika virus infectionVirus infectionZika virusAegypti salivary proteinsGuillain-Barre syndromeEarly inflammatory responseSkin of micePrevention of mosquitoInflammatory responseAedes aegypti mosquitoesTherapeutic measuresSalivary factorsSalivary proteinsMosquito-borneInfectionMiceSubstantial mortalityRecent epidemicProtein 1Aegypti mosquitoesAntigenic proteinsVirusAntibodiesMosquitoesAntiserumApobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat
Taura M, Song E, Ho YC, Iwasaki A. Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 2282-2289. PMID: 30670656, PMCID: PMC6369738, DOI: 10.1073/pnas.1819386116.Peer-Reviewed Original ResearchMeSH KeywordsCD4-Positive T-LymphocytesCell LineCytidine DeaminaseEpigenesis, GeneticGene Expression Regulation, ViralGene SilencingHIV InfectionsHIV Long Terminal RepeatHIV-1HumansNF-kappa BProtein BindingProtein Interaction Domains and MotifsProteinsSequence DeletionSp1 Transcription FactorVirus ActivationVirus LatencyConceptsHIV-1 latencyHIV-1 reactivationCD4 T cellsT cellsHuman primary CD4 T cellsInfected CD4 T cellsHIV-1-infected cellsPrimary CD4 T cellsLong terminal repeat regionHIV-1Therapeutic strategiesLower reactivationProviral DNALatency maintenanceTarget cellsLatency stateCell linesLong terminal repeatTerminal repeat regionMolecular mechanismsReactivationCellsKnockdownA3AUnexpected role