2020
Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation
Kang JW, Yan J, Ranjan K, Zhang X, Turner JR, Abraham C. Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation. Gastroenterology 2020, 159: 1051-1067. PMID: 32693188, PMCID: PMC8139320, DOI: 10.1053/j.gastro.2020.07.024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleHost Microbial InteractionsHumansImmunity, MucosalIntestinal MucosaIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutMyeloid CellsPrimary Cell CultureSalmonella InfectionsSalmonella typhimuriumConceptsIntestinal lymphoid organsBurden of bacteriaDextran sodium sulfateWild-type miceLymphoid organsTh17 cytokinesIntestinal inflammationDendritic cellsMyeloid cellsT cellsTh2 cytokinesMesenteric lymph node dendritic cellsLymph node dendritic cellsMyeloid cell-derived cytokinesAdaptive T cell responsesT cell transfer colitisMyeloid-specific disruptionInflammatory bowel diseaseReactive oxygen speciesImmune-mediated diseasesT cell responsesT helper 1Cell-derived cytokinesT cell cytokinesBone marrow-derived macrophagesT Cell-Intrinsic IRF5 Regulates T Cell Signaling, Migration, and Differentiation and Promotes Intestinal Inflammation
Yan J, Pandey SP, Barnes BJ, Turner JR, Abraham C. T Cell-Intrinsic IRF5 Regulates T Cell Signaling, Migration, and Differentiation and Promotes Intestinal Inflammation. Cell Reports 2020, 31: 107820. PMID: 32610123, PMCID: PMC7409536, DOI: 10.1016/j.celrep.2020.107820.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCell DifferentiationCell MovementColitisCytokinesGenetic Predisposition to DiseaseHumansInflammationInterferon Regulatory FactorsIntestinesLymph NodesMice, Inbred BALB CReceptors, Antigen, T-CellReceptors, ChemokineSignal TransductionT-LymphocytesUp-RegulationConceptsInflammatory outcomesTh17-associated transcription factorsMultiple immune-mediated diseasesPromotes Intestinal InflammationTh17-associated cytokinesAnti-inflammatory cytokinesImmune-mediated diseasesTh2-associated cytokinesChemokine-induced migrationExperimental colitisIntestinal inflammationUlcerative colitisHuman CD4IRF5 polymorphismsT cell signalingCytokinesCD4IRF5Th1Myeloid lineageGenetic carriersColitisCell migrationKey roleOutcomes
2016
IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation
Hedl M, Yan J, Abraham C. IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation. Cell Reports 2016, 16: 2442-2455. PMID: 27545875, PMCID: PMC5165654, DOI: 10.1016/j.celrep.2016.07.060.Peer-Reviewed Original ResearchMeSH KeywordsAcetylmuramyl-Alanyl-IsoglutamineAdjuvants, ImmunologicAnimalsCell DifferentiationGene Expression RegulationGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitInterferon Regulatory FactorsInterleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsMacrophagesMiceMice, Inbred C57BLMice, KnockoutMutationNod2 Signaling Adaptor ProteinPrimary Cell CultureProtein BindingProto-Oncogene Proteins c-aktReceptor-Interacting Protein Serine-Threonine Kinase 2Signal TransductionTNF Receptor-Associated Factor 6ConceptsInterferon regulatory factor 5Akt2 activationPro-inflammatory cytokinesM1 macrophage polarizationGlycolytic pathway genesHuman macrophagesDisease-associated polymorphismsM1 polarizationMacrophage polarizationInflammatory M1 macrophage polarizationPathway genesProximal signalingOligomerization domainRegulatory factor 5Glycolytic pathwayEnhanced glycolysisGenetic variantsGlycolysisMetabolic outcomesIRF5 expressionM1 macrophagesCentral mediatorFactor 5CytokinesMacrophages
2015
T Cell–Extrinsic CD18 Attenuates Antigen-Dependent CD4+ T Cell Activation In Vivo
Wu X, Lahiri A, Sarin R, Abraham C. T Cell–Extrinsic CD18 Attenuates Antigen-Dependent CD4+ T Cell Activation In Vivo. The Journal Of Immunology 2015, 194: 4122-4129. PMID: 25801431, PMCID: PMC4404034, DOI: 10.4049/jimmunol.1401328.Peer-Reviewed Original ResearchConceptsT cell activationCell proliferationAg-dependent T cell activationCell activationCell-extrinsic roleHematopoietic cellsEssential roleT cell proliferationCritical roleAdhesion moleculesΒ2 integrinsProliferationT cellsCellsActivationVivoActivation profilesAPCNaive T cellsSecondary lymphoid organsLeukocyte adhesion moleculesTraffickingRoleIntegrinsCD11b blockade
2014
Activation of Pattern Recognition Receptors Up-Regulates Metallothioneins, Thereby Increasing Intracellular Accumulation of Zinc, Autophagy, and Bacterial Clearance by Macrophages
Lahiri A, Abraham C. Activation of Pattern Recognition Receptors Up-Regulates Metallothioneins, Thereby Increasing Intracellular Accumulation of Zinc, Autophagy, and Bacterial Clearance by Macrophages. Gastroenterology 2014, 147: 835-846. PMID: 24960189, PMCID: PMC4170054, DOI: 10.1053/j.gastro.2014.06.024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Bacterial AgentsAutophagyCaspase 1Cells, CulturedDNA-Binding ProteinsGene Expression RegulationHumansIntestinal MucosaIntestinesMacrophagesMetallothioneinMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNod2 Signaling Adaptor ProteinRNA InterferenceTime FactorsToll-Like ReceptorsTranscription FactorsTransfectionZincConceptsMetal-regulatory transcription factor 1Human monocyte-derived macrophagesPattern recognition receptorsMonocyte-derived macrophagesIntracellular zincMyeloid-derived cellsSmall interfering RNAsBacterial clearanceGentamicin protection assaysInduction of autophagyTranscription factor 1Metallothionein geneMultiple genesInterfering RNAsIntestinal macrophagesSpecific proteinsOligomerization domain 2Domain 2Toll-like receptor 5AutophagyIntestinal lamina propria cellsContinuous stimulationSpecific pathogen-free facilityProtection assaysInduces expressionNOD2 Regulates CXCR3-Dependent CD8+ T Cell Accumulation in Intestinal Tissues with Acute Injury
Wu X, Lahiri A, Haines GK, Flavell RA, Abraham C. NOD2 Regulates CXCR3-Dependent CD8+ T Cell Accumulation in Intestinal Tissues with Acute Injury. The Journal Of Immunology 2014, 192: 3409-3418. PMID: 24591373, PMCID: PMC4064676, DOI: 10.4049/jimmunol.1302436.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalBone Marrow CellsCD3 ComplexCD8-Positive T-LymphocytesCell MovementCells, CulturedChemokine CXCL10Chemokine CXCL9ColitisDendritic CellsFlow CytometryGene ExpressionInterferon-gammaInterleukin-10Intestinal MucosaIntestinesMacrophagesMiceMice, Inbred C57BLMice, KnockoutModels, ImmunologicalNod2 Signaling Adaptor ProteinReceptors, CXCR3Reverse Transcriptase Polymerase Chain ReactionConceptsT cell accumulationT cell migrationT cell activationT cellsIntestinal injuryIntestinal tissueCell accumulationCell activationSmall intestinal lamina propriaIFN-γ neutralizationIntestinal T cellsT-cell depletionIntestinal immune homeostasisIL-10 productionT cell recruitmentHuman autoimmune diseasesIntestinal lamina propriaTreatment of miceIL-10 expressionIntestinal stromal cellsT cell outcomesCell migrationCXCR3 blockadeMAb administrationDendritic cells
2013
NF-κB1 Inhibits NOD2-Induced Cytokine Secretion through ATF3-Dependent Mechanisms
Zheng S, Abraham C. NF-κB1 Inhibits NOD2-Induced Cytokine Secretion through ATF3-Dependent Mechanisms. Molecular And Cellular Biology 2013, 33: 4857-4871. PMID: 24100018, PMCID: PMC3889551, DOI: 10.1128/mcb.00797-13.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 3AnimalsCells, CulturedCytokinesEpigenesis, GeneticGene Knockdown TechniquesHistonesHumansIleumMacrophagesMiceMice, Inbred C57BLMice, KnockoutNF-kappa B p50 SubunitNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinPrimary Cell CulturePromoter Regions, GeneticProtein Processing, Post-TranslationalToll-Like Receptor 2Toll-Like Receptor 4Transcriptional ActivationConceptsChronic NOD2 stimulationIntestinal immune homeostasisCytokine secretionNOD2 stimulationNF-κB1Immune homeostasisHuman macrophagesNF-κB pathwayNF-κB1 expressionCytokine downregulationInhibitory pathwaysNOD2ATF3 expressionSecretionIntestinal environmentGene promoterCytokine gene promotersStimulationInhibitory histone modificationsATF3MacrophagesKnockdown conditionsCritical mechanismHomeostasisCytokines
2012
IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine
Huber S, Gagliani N, Zenewicz LA, Huber FJ, Bosurgi L, Hu B, Hedl M, Zhang W, O’Connor W, Murphy AJ, Valenzuela DM, Yancopoulos GD, Booth CJ, Cho JH, Ouyang W, Abraham C, Flavell RA. IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine. Nature 2012, 491: 259-263. PMID: 23075849, PMCID: PMC3493690, DOI: 10.1038/nature11535.Peer-Reviewed Original Research
2009
Inflammatory Bowel Disease
Abraham C, Cho JH. Inflammatory Bowel Disease. New England Journal Of Medicine 2009, 361: 2066-2078. PMID: 19923578, PMCID: PMC3491806, DOI: 10.1056/nejmra0804647.Peer-Reviewed Original Research