2024
DHX9 maintains epithelial homeostasis by restraining R-loop-mediated genomic instability in intestinal stem cells
Ren X, Liu Q, Zhou P, Zhou T, Wang D, Mei Q, Flavell R, Liu Z, Li M, Pan W, Zhu S. DHX9 maintains epithelial homeostasis by restraining R-loop-mediated genomic instability in intestinal stem cells. Nature Communications 2024, 15: 3080. PMID: 38594251, PMCID: PMC11004185, DOI: 10.1038/s41467-024-47235-2.Peer-Reviewed Original ResearchConceptsInflammatory bowel diseaseIntestinal stem cellsIntestinal epithelial cellsEpithelial homeostasisSusceptibility to experimental colitisIncreased susceptibility to experimental colitisImpaired ISC functionStem cellsEpithelial barrier dysfunctionGenomic instabilityInflammatory bowel disease patientsPathogenesis of inflammatory bowel diseaseR-loop-mediated genome instabilityHallmarks of inflammatory bowel diseaseContinuous self-renewalBarrier dysfunctionExperimental colitisCrypt destructionEpithelial cellsInflammatory responseSelf-renewalBowel diseaseRisk factorsIntestinal epitheliumProtein levels
2020
T 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
2015
Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells
Hernandez AL, Kitz A, Wu C, Lowther DE, Rodriguez DM, Vudattu N, Deng S, Herold KC, Kuchroo VK, Kleinewietfeld M, Hafler DA. Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells. Journal Of Clinical Investigation 2015, 125: 4212-4222. PMID: 26524592, PMCID: PMC4639983, DOI: 10.1172/jci81151.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAntibodies, NeutralizingAutoimmunityCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitisCytokinesForkhead Transcription FactorsGene Expression ProfilingGenes, ReporterGraft vs Host DiseaseHeterograftsHumansImmediate-Early ProteinsInflammationInterferon-gammaLeukocytes, MononuclearMaleMiceProtein Serine-Threonine KinasesRNA InterferenceRNA, Small InterferingSodium ChlorideSodium Chloride, DietaryT-Lymphocytes, RegulatoryConceptsHigh-salt dietTreg functionIFNγ secretionCD4 effector cellsHuman Treg functionRegulatory T cellsAdoptive transfer modelAnti-IFNγ antibodyHost disease modelType 1 diabetesInduction of proinflammatoryTreg pathwayExperimental colitisXenogeneic graftEffector cellsMultiple sclerosisProinflammatory responseT cellsTregsMurine modelSuppressive activitySuppressive functionSerum/glucocorticoid-regulated kinaseAutoimmunityGlucocorticoid-regulated kinase
2013
Intestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer
Xie Y, Matsumoto H, Nalbantoglu I, Kerr TA, Luo J, Rubin DC, Kennedy S, Davidson NO. Intestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer. PLOS ONE 2013, 8: e67819. PMID: 23805328, PMCID: PMC3689718, DOI: 10.1371/journal.pone.0067819.Peer-Reviewed Original ResearchConceptsMttp-IKO miceDextran sodium sulfateDSS treatmentExperimental colitisTumor burdenColitis-Associated CancerDevelopment of colitisIndependent risk factorDietary fat intakeColonic mRNA expressionLevels of TNFαColonic tumor burdenIntestine-specific deletionMicrosomal triglyceride transfer proteinDSS administrationColonic inflammationColonic injuryIL-17AInflammasome expressionSystemic injuryFat intakeFat malabsorptionColorectal cancerCytokine expressionIL-1β
2006
Caveolin‐1 regulation of experimental colitis
Greer J, Chidlow J, Bernatchez P, Sessa W, Shukla D, Kevil C. Caveolin‐1 regulation of experimental colitis. The FASEB Journal 2006, 20: a1378-a1378. DOI: 10.1096/fasebj.20.5.a1378.Peer-Reviewed Original ResearchDisease activity indexExperimental colitisAP-CavDextran sulfate sodium (DSS) modelWild-type control miceDSS-Induced ColitisInflammatory bowel diseaseCaveolin-1Degree of inflammationWild-type miceWild-type colonAB peptideGross bleedingTransmural inflammationInduced colitisMicrovascular dysfunctionStool consistencyBowel diseaseMicrovascular functionLymphoplasmacytic infiltrateOccult bloodControl miceHistopathology scoresInflammatory responseColitis
2001
Development of chronic colitis is dependent on the cytokine MIF
de Jong Y, Abadia-Molina A, Satoskar A, Clarke K, Rietdijk S, Faubion W, Mizoguchi E, Metz C, Sahli M, ten Hove T, Keates A, Lubetsky J, Farrell R, Michetti P, van Deventer S, Lolis E, David J, Bhan A, Terhorst C. Development of chronic colitis is dependent on the cytokine MIF. Nature Immunology 2001, 2: 1061-1066. PMID: 11668338, DOI: 10.1038/ni720.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAutoimmune DiseasesBone Marrow TransplantationChronic DiseaseColitisCrohn DiseaseDNA-Binding ProteinsFemaleHumansImmunization, PassiveLipopolysaccharidesMacrophage ActivationMacrophage Migration-Inhibitory FactorsMaleMiceMice, KnockoutModels, AnimalNuclear ProteinsRadiation ChimeraWeight LossConceptsMacrophage migration inhibitory factorCytokine macrophage migration inhibitory factorMIF-deficient miceCrohn's diseaseRole of MIFImmune systemPlasma MIF concentrationMucosal immune systemInnate immune cellsInnate immune systemChronic colitisMIF concentrationsExperimental colitisMIF productionMurine colitisImmune cellsColitisIntestinal bacteriaInhibitory factorDiseaseNew targetsMiceLipopolysaccharideCell typesPatients
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