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
2008
Transduction of the cytoplasmic domain of CTLA-4 inhibits TcR-specific activation signals and prevents collagen-induced arthritis
Choi JM, Kim SH, Shin JH, Gibson T, Yoon BS, Lee DH, Lee SK, Bothwell AL, Lim JS, Lee SK. Transduction of the cytoplasmic domain of CTLA-4 inhibits TcR-specific activation signals and prevents collagen-induced arthritis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 19875-19880. PMID: 19066215, PMCID: PMC2604944, DOI: 10.1073/pnas.0805198105.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisT cell activationCTLA-4Human umbilical vein endothelial cellsCell activationInflammatory cytokine productionErosion of cartilageCytoplasmic domainEffective therapeutic approachActivated T cellsUmbilical vein endothelial cellsCell-permeable formT cell receptor-proximal signalingVein endothelial cellsAntibody levelsRheumatoid arthritisAutoimmune diseasesCytokine productionHuman CTLT cellsTherapeutic approachesCell-permeable recombinant proteinArthritisTransdermal administrationMouse T cell activation
2004
Interferon α but Not Interleukin 12 Activates STAT4 Signaling in Human Vascular Endothelial Cells*
Torpey N, Maher SE, Bothwell AL, Pober JS. Interferon α but Not Interleukin 12 Activates STAT4 Signaling in Human Vascular Endothelial Cells*. Journal Of Biological Chemistry 2004, 279: 26789-26796. PMID: 15087447, DOI: 10.1074/jbc.m401517200.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorCells, CulturedChemokine CCL2DNADNA, ComplementaryDNA-Binding ProteinsDose-Response Relationship, DrugEndothelium, VascularEnzyme-Linked Immunosorbent AssayFlow CytometryHumansImmunoblottingInflammationInterferon-alphaInterleukin-12Oligonucleotide Array Sequence AnalysisPhosphorylationPrecipitin TestsProtein Structure, TertiaryRecombinant ProteinsRepressor ProteinsRetroviridaeReverse Transcriptase Polymerase Chain ReactionRNARNA, MessengerSignal TransductionSTAT4 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTime FactorsTrans-ActivatorsTranscription FactorsUmbilical VeinsUp-RegulationConceptsHuman umbilical vein ECMonocyte chemoattractant protein-1Quantitative RT-PCRVascular endothelial cellsEndothelial cellsChemokine monocyte chemoattractant protein-1Chemoattractant protein-1Cultured human umbilical vein endothelial cellsPro-inflammatory behaviorIFNalpha responseHuman vascular endothelial cellsHuman umbilical vein endothelial cellsUmbilical vein endothelial cellsNeuroblastoma cell linesSuppressor of cytokineVein endothelial cellsEffector cellsInterleukin-12T cellsSTAT4 pathwayInterferon αIL12 receptorCytokinesU3A cellsRT-PCR