Jin-Young Choi, PhD
Research Scientist (Rheumatology, Allergy & Immunology)Cards
About
Research
Publications
2025
The gut microbiota limits systemic inflammation during neurotrophic viral CNS infection by priming tonic type I interferon signaling
Cho H, Byeon H, Park S, Uyangaa E, Choi J, Kim K, Eo S. The gut microbiota limits systemic inflammation during neurotrophic viral CNS infection by priming tonic type I interferon signaling. Journal Of Neuroinflammation 2025, 22: 259. PMID: 41189008, PMCID: PMC12584447, DOI: 10.1186/s12974-025-03579-0.Peer-Reviewed Original ResearchConceptsCentral nervous systemSystemic inflammationFecal microbiota transplantationCentral nervous system neuroinflammationBlood-brain barrierJapanese encephalitis virusCNS neuroinflammationViral disseminationInfiltration of peripheral immune cellsDepletion of gut microbiotaViral CNS infectionsGut microbiotaPeripheral immune cellsSystemic immune responsesNeurotropic viral infectionsType I Interferon SignalingAntibiotic cocktail treatmentExtraneural tissuesJapanese encephalitis virus infectionI interferon signalingIFN-I responseType I interferonCNS infectionOrgan injuryImmune cellsMyeloid cAMP Reduction Shifts Rhinovirus‐Induced Airway Inflammation From Neutrophilic to Eosinophilic by Suppressing M1‐Interstitial Macrophages
Park S, Uyangaa E, Kim H, Byeon H, Choi J, Kim K, Lee J, Bertin S, Raz E, Eo S. Myeloid cAMP Reduction Shifts Rhinovirus‐Induced Airway Inflammation From Neutrophilic to Eosinophilic by Suppressing M1‐Interstitial Macrophages. Allergy 2025, 80: 3055-3076. PMID: 40878403, PMCID: PMC12590349, DOI: 10.1111/all.70018.Peer-Reviewed Original ResearchConceptsHRV-induced asthma exacerbationsHuman rhinovirus infectionAirway inflammationAsthma exacerbationsCAMP levelsHuman rhinovirusAdoptive transferM1 polarizationNLRP3 inflammasome activationEffector cell expansionMyeloid cell-specific deletionNeutrophil-dominated airway inflammationCell-specific deletionReduction of cAMPInflammasome activationTh2-type inflammationAssociated with M1 polarizationLung function impairmentSignificant healthcare costsSteroid resistanceAllergen challengeEosinophilic inflammationCorticosteroid responseEosinophilic phenotypeMyeloid cellsThe ERVK3‑1 Microprotein Interacts with the HUSH Complex
Jayatissa A, Jaunbocus N, Erkalo B, Jiang K, Zheng S, Su H, Yan L, Choi J, Vaughan J, Bacchiocchi A, Na Z, Cao X, Halaban R, Saghatelian A, Craft J, Chen Y, Slavoff S. The ERVK3‑1 Microprotein Interacts with the HUSH Complex. Biochemistry 2025, 64: 3372-3381. PMID: 40699144, PMCID: PMC12339190, DOI: 10.1021/acs.biochem.5c00023.Peer-Reviewed Original ResearchConceptsHUSH complexTranscriptional repressionHuman endogenous retrovirusesIntron-less geneRegulation of target gene expressionEndogenous retrovirusesTarget gene expressionGenomic elementsHuman genomeTarget genesGene expressionHuman cellsMicroproteinsExogenous retrovirusesLociGenesRetrovirusesRetrotransposonsGenomeMolecular remnantsRepressionPPHLN1ComplexRegulation
2024
Inhibition of NADPH oxidase 2 enhances resistance to viral neuroinflammation by facilitating M1-polarization of macrophages at the extraneural tissues
Choi J, Byeon H, Park S, Uyangaa E, Kim K, Eo S. Inhibition of NADPH oxidase 2 enhances resistance to viral neuroinflammation by facilitating M1-polarization of macrophages at the extraneural tissues. Journal Of Neuroinflammation 2024, 21: 115. PMID: 38698374, PMCID: PMC11067137, DOI: 10.1186/s12974-024-03078-8.Peer-Reviewed Original ResearchConceptsAccumulation of M1 macrophagesCentral nervous systemJE progressionT cell responsesViral loadJE virus infectionMacrophage polarizationM1 macrophage polarizationReactive oxygen speciesBone marrowJE virusRegulation of macrophage polarizationCD8+ T cell responsesM1 macrophagesExtraneural tissuesSuppression of viral replicationInhibition of NADPH oxidase 2NOX2-deficient miceInfiltration of inflammatory cellsPeripheral lymphoid tissuesM1 macrophage accumulationNADPH oxidase-derived reactive oxygen speciesNADPH oxidase 2Japanese encephalitisM1 polarization of macrophages
2023
TLR3/TRIF pathway confers protection against herpes simplex encephalitis through NK cell activation mediated by a loop of type I IFN and IL‐15 from epithelial and dendritic cells
Uyangaa E, Choi J, Park S, Byeon H, Cho H, Kim K, Eo S. TLR3/TRIF pathway confers protection against herpes simplex encephalitis through NK cell activation mediated by a loop of type I IFN and IL‐15 from epithelial and dendritic cells. Immunology 2023, 170: 83-104. PMID: 37278103, DOI: 10.1111/imm.13664.Peer-Reviewed Original ResearchConceptsNK cell activityHerpes simplex encephalitisHSE progressionImpaired NK cell activityDendritic cellsCell activationVaginal tractHSV-1IFN-IIL-15Epithelial cellsGenetic causeEpithelial layerBone marrow transplantationIL-15 productionHerpes simplex virus type 1Tissue-resident cellsHSV-1 infectionVirus type 1IFN-I receptorResponse to IFN-IProtective roleGlobal cerebral dysfunctionType I IFNIFN-I productionAP-1–independent NFAT signaling maintains follicular T cell function in infection and autoimmunity
Seth A, Yokokura Y, Choi J, Shyer J, Vidyarthi A, Craft J. AP-1–independent NFAT signaling maintains follicular T cell function in infection and autoimmunity. Journal Of Experimental Medicine 2023, 220: e20211110. PMID: 36820828, PMCID: PMC9998660, DOI: 10.1084/jem.20211110.Peer-Reviewed Original ResearchConceptsTfh cellsT cellsFollicular helper T cellsLupus-prone miceT cell subsetsTfh cell developmentHelper T cellsHumoral immune responseT cell functionGerminal center B cellsT cell statesRenal injuryAutoantibody productionCell subsetsPrimary T cellsImmune responseB cellsPharmacologic inhibitionTherapeutic insightsCell functionGenetic disruptionNFATCell developmentCellsGene expression
2022
SARS‐CoV‐2 infection in severe asthma is associated with worsening of COVID‐19 through respiratory NLRP3 inflammasome activation
Jeong J, Choi J, Kim J, Park S, Kim W, Yoon Y, Park H, Park K, Kim D, Kim J, Koh G, Eo S, Lee Y. SARS‐CoV‐2 infection in severe asthma is associated with worsening of COVID‐19 through respiratory NLRP3 inflammasome activation. Allergy 2022, 78: 287-290. PMID: 35871401, PMCID: PMC9349818, DOI: 10.1111/all.15452.Commentaries, Editorials and LettersT cell‐intrinsic miR‐155 is required for Th2 and Th17‐biased responses in acute and chronic airway inflammation by targeting several different transcription factors
Kim H, Park S, Byeon H, Eo J, Choi J, Tanveer M, Uyangaa E, Kim K, Eo S. T cell‐intrinsic miR‐155 is required for Th2 and Th17‐biased responses in acute and chronic airway inflammation by targeting several different transcription factors. Immunology 2022, 166: 357-379. PMID: 35404476, DOI: 10.1111/imm.13477.Peer-Reviewed Original ResearchConceptsDeficiency of miR-155Neutrophilic airway inflammationCell-intrinsic roleAirway inflammationT cellsRegulation of adaptive T cell responsesTh17-mediated airway inflammationCell activationAdaptive T cell responsesAllergen exposureTh2 cell activationT cell responsesAcute allergen exposureEosinophilic airway inflammationTh17 cell activationAsthmatic airway inflammationChronic airway inflammationTh17-biased responseFunctional activityExpression of c-MafMiR-155Th2-mediatedTh17 cellsTh17-typeAsthma model
2021
Experimental infection of dogs with severe fever with thrombocytopenia syndrome virus: Pathogenicity and potential for intraspecies transmission
Park S, Park J, Choi J, Oh B, Yang M, Lee S, Kim J, Eo S, Chae J, Lim C, Oem J, Tark D, Kim B. Experimental infection of dogs with severe fever with thrombocytopenia syndrome virus: Pathogenicity and potential for intraspecies transmission. Transboundary And Emerging Diseases 2021, 69: 3090-3096. PMID: 34716981, DOI: 10.1111/tbed.14372.Peer-Reviewed Original ResearchConceptsDays post-infectionExperimental infectionExperimental infection of dogsSFTSV transmissionInfection of dogsSevere feverViral RNAInfected dogsThrombocytopenia syndrome virusContact dogsImmunocompetent dogsImmunosuppressed dogsPost-infectionIntramuscular inoculationZoonotic diseaseIntraspecies transmissionDogsDabie bandavirusSFTSVWeight lossThrombocytopenia syndromeExperiment 1Experiment 2Co-housingNeutralizing antibodiesType I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b+Ly-6C+ monocytes
Patil A, Choi J, Park S, Uyangaa E, Kim B, Kim K, Eo S. Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b+Ly-6C+ monocytes. Journal Of Neuroinflammation 2021, 18: 136. PMID: 34130738, PMCID: PMC8204625, DOI: 10.1186/s12974-021-02180-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD11b AntigenCentral Nervous SystemCytokine Release SyndromeDisease Models, AnimalEncephalitis Virus, JapaneseEncephalitis, JapaneseHemorrhageHost-Pathogen InteractionsInflammation MediatorsInterferon Type ILymphoid TissueMiceMice, Inbred C57BLMice, KnockoutMonocytesReceptor, Interferon alpha-betaSignal TransductionViral TropismConceptsCentral nervous systemJEV inoculationTissue-resident cellsBone marrowIFN-IJapanese encephalitis virusCytokine productionIFN-I signalingViral disseminationVascular leakageImpaired inductionPeripheral organsTissue tropismUncontrolled cytokine productionType I IFN signalingInfection in vivoExcessive cytokine productionCentral nervous system neuroinflammationDissemination to peripheral organsAntiviral IFN-stimulated genesChimeric modelType I interferonNeurotrophic flavivirusBM cellsIFN-stimulated genes
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