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
2014
Human monocytes have increased IFN-γ-mediated IL-15 production with age alongside altered IFN-γ receptor signaling
Lee N, Shin MS, Kang KS, Yoo SA, Mohanty S, Montgomery RR, Shaw AC, Kang I. Human monocytes have increased IFN-γ-mediated IL-15 production with age alongside altered IFN-γ receptor signaling. Clinical Immunology 2014, 152: 101-110. PMID: 24657713, PMCID: PMC4018768, DOI: 10.1016/j.clim.2014.03.003.Peer-Reviewed Original Research
1999
Induction of Ig light chain gene rearrangement in heavy chain-deficient B cells by activated Ras
Shaw A, Swat W, Davidson L, Alt F. Induction of Ig light chain gene rearrangement in heavy chain-deficient B cells by activated Ras. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 2239-2243. PMID: 10051625, PMCID: PMC26767, DOI: 10.1073/pnas.96.5.2239.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBlastocystB-LymphocytesCell DifferentiationDNA-Binding ProteinsEmbryo, MammalianGene Rearrangement, B-Lymphocyte, Light ChainGenes, ImmunoglobulinImmunoglobulin Heavy ChainsImmunoglobulin kappa-ChainsImmunoglobulin Light ChainsImmunoglobulin Variable RegionKidneyMiceMolecular Sequence DataRas ProteinsRecombinant Fusion ProteinsSignal TransductionSpleenStem CellsTransfectionConceptsRas expressionVariable region gene assemblyEmbryonic stem cellsIg light chain gene rearrangementGene rearrangementsB cell developmentWild-type B cellsB lineage cellsLight chain gene rearrangementsDevelopmental checkpointsHeavy chain geneGene productsGene assemblyExpression constructsB cell differentiationGene expressionBlastocyst complementationIg heavy chain genesCell developmentCell differentiationVariable region genesB cellsDifferentiation potentialLineage cellsChain gene