2022
Combining Cellular Immunology With RNAseq to Identify Novel Chlamydia T-Cell Subset Signatures
Johnson RM, Asashima H, Mohanty S, Shaw AC. Combining Cellular Immunology With RNAseq to Identify Novel Chlamydia T-Cell Subset Signatures. The Journal Of Infectious Diseases 2022, 225: 2033-2042. PMID: 35172331, PMCID: PMC9159333, DOI: 10.1093/infdis/jiac051.Peer-Reviewed Original ResearchConceptsProtective T cell clonesAntibacterial effector mechanismsT cells residentB cell helpT cell clonesCytokine polarizationImmune miceIL-10Protective immunityVaccine trialsIL-13Surrogate biomarkerEffector mechanismsGenital tractT cellsVaccine candidatesChlamydia trachomatisCells residentHelper functionCellular immunologyMouse studiesHuman investigationsReproductive tractGranzyme A.Investigational data
2015
Paradoxical changes in innate immunity in aging: recent progress and new directions
Montgomery RR, Shaw AC. Paradoxical changes in innate immunity in aging: recent progress and new directions. Journal Of Leukocyte Biology 2015, 98: 937-943. PMID: 26188078, PMCID: PMC4661037, DOI: 10.1189/jlb.5mr0315-104r.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsB-LymphocytesCytokinesHumansImmunity, InnateSignal TransductionT-LymphocytesConceptsImmune responseInnate immune changesInnate immune responseCytokine levelsInappropriate elevationImmune changesNaïve cell populationT cellsAdaptive immunityViral infectionParadoxical increaseInnate immunityMultiple cell typesParadoxical changesCell populationsActivation stateImmunityCell typesSevere consequencesResponseTissue contextImmunosenescenceVaccinationPopulationInfection
2008
Defective signal transduction in B lymphocytes lacking presenilin proteins
Yagi T, Giallourakis C, Mohanty S, Scheidig C, Shen J, Zheng H, Xavier RJ, Shaw AC. Defective signal transduction in B lymphocytes lacking presenilin proteins. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 979-984. PMID: 18195359, PMCID: PMC2242696, DOI: 10.1073/pnas.0707755105.Peer-Reviewed Original ResearchConceptsPresenilin proteinsDiverse cellular processesMultiple genomic datasetsPS proteinsSignal transduction eventsWhole-genome datasetsDefective signal transductionNotch family membersCalcium-dependent signalingCellular processesProtein substratesSignal transductionTransduction eventsProtein interactionsPS2 functionUnanticipated roleConditional alleleGenomic datasetsToll-like receptor signalingPathway analysisIntegrative analysisPosttranslational cleavageReceptor signalingRecombinase expressionProtein
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 KeywordsAnimalsB-LymphocytesBase SequenceBlastocystCell 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 geneActivated Ras Signals Developmental Progression of Recombinase-activating Gene (RAG)-deficient Pro-B Lymphocytes
Shaw A, Swat W, Ferrini R, Davidson L, Alt F. Activated Ras Signals Developmental Progression of Recombinase-activating Gene (RAG)-deficient Pro-B Lymphocytes. Journal Of Experimental Medicine 1999, 189: 123-129. PMID: 9874569, PMCID: PMC1887686, DOI: 10.1084/jem.189.1.123.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesCell DifferentiationCell SurvivalDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation, DevelopmentalGenes, RAG-1Immunoglobulin Heavy ChainsImmunoglobulin kappa-ChainsMiceMice, KnockoutPhenotypeRas ProteinsRNA, MessengerStem CellsTranscription, GeneticUp-RegulationConceptsB cellsRAG-deficient backgroundPeripheral lymphoid tissuesB-cell lineageEarly B cell developmentB lineage cellsLymphoid tissueBcl-2 transgeneCD43 expressionRecombination-activating gene 1B cell developmentHeavy chain transgeneSurface markersB cell stageLineage cellsIntracellular pathwaysMature B-cell stageDeficient backgroundProgressionGene 1Survival signalsCell developmentOverall phenotypeResult of expressionCell lineages
1990
Mutations of immunoglobulin transmembrane and cytoplasmic domains: Effects on intracellular signaling and antigen presentation
Shaw A, Mitchell R, Weaver Y, Campos-Torres J, Abbas A, Leder P. Mutations of immunoglobulin transmembrane and cytoplasmic domains: Effects on intracellular signaling and antigen presentation. Cell 1990, 63: 381-392. PMID: 2119890, DOI: 10.1016/0092-8674(90)90171-a.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntibody FormationAntigensBase SequenceB-LymphocytesCalciumCell LineCell MembraneCytoplasmHumansImmunoglobulin mu-ChainsKineticsMiceMolecular Sequence DataMutagenesis, Site-DirectedOligonucleotide ProbesReceptors, Antigen, B-CellSequence Homology, Nucleic AcidSignal TransductionTransfectionConceptsCytoplasmic domainSignal transductionShort cytoplasmic domainDifferent protein interactionsMembrane-bound formMu chain geneProtein interactionsTransmembrane residuesIntracellular signalingChain geneSpecific mutationsTransductionAntigen presentationAntigen-specific receptorsMutationsTransmembraneB cellsGenesSignalingDomainResiduesCellsAssaysReceptors
1988
A human immunoglobulin gene reduces the incidence of lymphomas in c-Myc-bearing transgenic mice
Nussenzweig M, Schmidt E, Shaw A, Sinn E, Campos-Torres J, Mathey-Prevot B, Pattengale P, Leder P. A human immunoglobulin gene reduces the incidence of lymphomas in c-Myc-bearing transgenic mice. Nature 1988, 336: 446-450. PMID: 3143076, DOI: 10.1038/336446a0.Peer-Reviewed Original ResearchMeSH KeywordsAbelson murine leukemia virusAnimalsB-LymphocytesBone MarrowCell Transformation, NeoplasticCell Transformation, ViralEnhancer Elements, GeneticGenes, ImmunoglobulinHematopoietic Stem CellsHumansImmunoglobulin mu-ChainsLymphomaMiceMice, TransgenicPhenotypeProto-Oncogene ProteinsProto-Oncogene Proteins c-mycProto-OncogenesRNA, Messenger