2022
Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19
Unterman A, Sumida TS, Nouri N, Yan X, Zhao AY, Gasque V, Schupp JC, Asashima H, Liu Y, Cosme C, Deng W, Chen M, Raredon MSB, Hoehn KB, Wang G, Wang Z, DeIuliis G, Ravindra NG, Li N, Castaldi C, Wong P, Fournier J, Bermejo S, Sharma L, Casanovas-Massana A, Vogels CBF, Wyllie AL, Grubaugh ND, Melillo A, Meng H, Stein Y, Minasyan M, Mohanty S, Ruff WE, Cohen I, Raddassi K, Niklason L, Ko A, Montgomery R, Farhadian S, Iwasaki A, Shaw A, van Dijk D, Zhao H, Kleinstein S, Hafler D, Kaminski N, Dela Cruz C. Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19. Nature Communications 2022, 13: 440. PMID: 35064122, PMCID: PMC8782894, DOI: 10.1038/s41467-021-27716-4.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAgedAntibodies, Monoclonal, HumanizedCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedCOVID-19COVID-19 Drug TreatmentFemaleGene Expression ProfilingGene Expression RegulationHumansImmunity, InnateMaleReceptors, Antigen, B-CellReceptors, Antigen, T-CellRNA-SeqSARS-CoV-2Single-Cell AnalysisConceptsProgressive COVID-19B cell clonesSingle-cell analysisT cellsImmune responseMulti-omics single-cell analysisCOVID-19Cell clonesAdaptive immune interactionsSevere COVID-19Dynamic immune responsesGene expressionSARS-CoV-2 virusAdaptive immune systemSomatic hypermutation frequenciesCellular effectsProtein markersEffector CD8Immune signaturesProgressive diseaseHypermutation frequencyProgressive courseClassical monocytesClonesImmune interactions
2019
Integrating multiomics longitudinal data to reconstruct networks underlying lung development
Ding J, Ahangari F, Espinoza CR, Chhabra D, Nicola T, Yan X, Lal CV, Hagood JS, Kaminski N, Bar-Joseph Z, Ambalavanan N. Integrating multiomics longitudinal data to reconstruct networks underlying lung development. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2019, 317: l556-l568. PMID: 31432713, PMCID: PMC6879899, DOI: 10.1152/ajplung.00554.2018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornChildChild, PreschoolDNA MethylationEpigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHumansImmunity, InnateInfantInfant, NewbornLungMaleMiceMice, Inbred C57BLMicroRNAsOrganogenesisProteomicsPulmonary AlveoliRNA, MessengerSingle-Cell AnalysisTranscriptomeConceptsSingle-cell RNA-seq dataLung developmentDynamic regulatory networksOmics data setsRNA-seq dataIndividual cell typesHuman lung developmentRegulatory networksDNA methylationLaser capture microdissectionEpigenetic changesExpression trajectoriesKey pathwaysCell typesActive pathwaysCapture microdissectionRegulatorKey eventsInnate immunityNew insightsSpecific key eventsPathwayComprehensive understandingProteomicsMethylation
2014
T cell-intrinsic role of IL-6 signaling in primary and memory responses
Nish SA, Schenten D, Wunderlich FT, Pope SD, Gao Y, Hoshi N, Yu S, Yan X, Lee HK, Pasman L, Brodsky I, Yordy B, Zhao H, Brüning J, Medzhitov R. T cell-intrinsic role of IL-6 signaling in primary and memory responses. ELife 2014, 3: e01949. PMID: 24842874, PMCID: PMC4046568, DOI: 10.7554/elife.01949.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesDose-Response Relationship, DrugImmunity, InnateImmunizationImmunologic MemoryInterleukin-1betaInterleukin-6Interleukin-6 Receptor alpha SubunitMice, Inbred C57BLMice, KnockoutOvalbuminRecombinant ProteinsSignal TransductionTh1 CellsTh17 CellsT-Lymphocytes, RegulatoryConceptsIL-6T cellsIL-6 receptor α chainT cell memory formationT cell-intrinsic roleAbsence of TregsDepletion of TregsPrimary Th1 responseEffector T cellsT cell responsesFunctional memory cellsAdaptive immune responsesT cell-specific deletionInnate immune recognitionCell-intrinsic roleCell-specific deletionReceptor α chainTfh functionTh1 responseTh17 responsesIL-1βIL-2Immune responseTregsSuppressive effectSignaling through the Adaptor Molecule MyD88 in CD4+ T Cells Is Required to Overcome Suppression by Regulatory T Cells
Schenten D, Nish SA, Yu S, Yan X, Lee HK, Brodsky I, Pasman L, Yordy B, Wunderlich FT, Brüning JC, Zhao H, Medzhitov R. Signaling through the Adaptor Molecule MyD88 in CD4+ T Cells Is Required to Overcome Suppression by Regulatory T Cells. Immunity 2014, 40: 78-90. PMID: 24439266, PMCID: PMC4445716, DOI: 10.1016/j.immuni.2013.10.023.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsCells, CulturedImmunity, InnateImmunologic MemoryImmunosuppression TherapyInterleukin-1Interleukin-18MiceMice, Inbred C57BLMice, TransgenicMyeloid Differentiation Factor 88Organ SpecificityReceptors, Interleukin-1Signal TransductionTh1 CellsTh17 CellsT-Lymphocytes, RegulatoryConceptsToll-like receptorsTh1 cell responsesT cellsCell-specific ablationCell responsesIL-1Interleukin-1 receptor family memberT helper 17 (Th17) cell responsesTreg cell-mediated suppressionTreg cell-specific ablationT cell-specific ablationRegulatory T cellsT regulatory (Treg) cellsCell-mediated suppressionMemory T cellsAdaptor molecule MyD88Adaptive immune responsesIL-1 actsTreg cellsRegulatory cellsReceptor family membersMolecule MyD88Th1 cellsImmune responseMyD88