2018
Intranuclear delivery of the transcription modulation domain of Tbet-improved lupus nephritis in (NZB/NZW) F1 lupus-prone mice
Moon JS, Mun CH, Kim JH, Cho JY, Park SD, Park TY, Shin JS, Ho CC, Park YB, Ghosh S, Bothwell ALM, Lee SW, Lee SK. Intranuclear delivery of the transcription modulation domain of Tbet-improved lupus nephritis in (NZB/NZW) F1 lupus-prone mice. Kidney International 2018, 93: 1118-1130. PMID: 29409726, DOI: 10.1016/j.kint.2017.11.017.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsAnti-Inflammatory AgentsCell NucleusCellular MicroenvironmentCytokinesDisease Models, AnimalFemaleInflammation MediatorsKidneyLupus NephritisMice, Inbred NZBProtein DomainsRecombinant ProteinsSpleenT-Box Domain ProteinsT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryTranscription, GeneticConceptsLupus-prone miceTranscription modulation domainSystemic lupus erythematosusCell subsetsTh1-mediated autoimmune diseasesNucleus-transducible formNumber of Th1Severity of nephritisT cell subsetsT cell activationProinflammatory microenvironmentTh17 cellsTreg cellsImmunosuppressive cytokinesLupus patientsLupus erythematosusAutoimmune diseasesImmune therapeuticsF1 miceCell activationExcessive expressionMiceTbetMarked increaseMethylprednisolone
2016
Sex-Based Selectivity of PPARγ Regulation in Th1, Th2, and Th17 Differentiation
Park HJ, Park HS, Lee JU, Bothwell AL, Choi JM. Sex-Based Selectivity of PPARγ Regulation in Th1, Th2, and Th17 Differentiation. International Journal Of Molecular Sciences 2016, 17: 1347. PMID: 27548145, PMCID: PMC5000743, DOI: 10.3390/ijms17081347.Peer-Reviewed Original ResearchConceptsEffector T cell differentiationT cellsT cell differentiationAdaptive immunityFemale T cellsMale T cellsPeroxisome proliferator-activated receptor gammaIL-17 productionDifferentiation of Th1PPARγ agonist pioglitazoneProliferator-activated receptor gammaNaïve T cellsSplenic T cellsMouse splenic T cellsImportant immune regulatorPioglitazone treatmentTfh responsesTh17 cellsAgonist pioglitazoneTreg functionAutoimmune diseasesEstrogen exposureImmune regulatorsCell differentiationTh1
2009
Transforming growth factor β is dispensable for the molecular orchestration of Th17 cell differentiation
Das J, Ren G, Zhang L, Roberts AI, Zhao X, Bothwell AL, Van Kaer L, Shi Y, Das G. Transforming growth factor β is dispensable for the molecular orchestration of Th17 cell differentiation. Journal Of Experimental Medicine 2009, 206: 2407-2416. PMID: 19808254, PMCID: PMC2768861, DOI: 10.1084/jem.20082286.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCytokinesEncephalomyelitis, Autoimmune, ExperimentalGATA3 Transcription FactorInterleukin-6Lymphocyte ActivationMiceMice, KnockoutSTAT4 Transcription FactorSTAT6 Transcription FactorT-Box Domain ProteinsTh1 CellsTh2 CellsT-Lymphocytes, Helper-InducerTransforming Growth Factor betaConceptsTh17 cell differentiationTh17 cellsIL-6Wild-type BALB/c miceBALB/c miceTh17-specific transcription factorsExperimental autoimmune encephalomyelitisT helper cellsCell differentiationGrowth factor betaTh2 cell differentiationGrowth factor βC-STATAutoimmune encephalomyelitisAntiinflammatory cytokinesAutoimmune disordersProinflammatory cytokinesHelper cellsBeta antibodyC miceTh2 cellsFactor betaGATA-3CytokinesMice