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
2014
Mutation of POLB Causes Lupus in Mice
Senejani AG, Liu Y, Kidane D, Maher SE, Zeiss CJ, Park HJ, Kashgarian M, McNiff JM, Zelterman D, Bothwell AL, Sweasy JB. Mutation of POLB Causes Lupus in Mice. Cell Reports 2014, 6: 1-8. PMID: 24388753, PMCID: PMC3916967, DOI: 10.1016/j.celrep.2013.12.017.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusLupus-like diseaseLupus erythematosusAutoimmune pathologyMouse modelGenome-wide association studiesPol β activityDecreased expressionMutant miceUnderlying causeMicePrevious genome-wide association studyΒ activityDNA polymerase activityReplication studyExcision repair pathwayImmune diversitySomatic hypermutationBase excision repair pathwayAssociation studiesErythematosusLupusPolymerase activityExpressionKey enzyme
2011
IL-17F deficiency inhibits small intestinal tumorigenesis in ApcMin/+ mice
Chae WJ, Bothwell AL. IL-17F deficiency inhibits small intestinal tumorigenesis in ApcMin/+ mice. Biochemical And Biophysical Research Communications 2011, 414: 31-36. PMID: 21939640, DOI: 10.1016/j.bbrc.2011.09.016.Peer-Reviewed Original ResearchConceptsIL-17FSpontaneous intestinal tumorigenesisIntestinal tumorigenesisLamina propriaCD4 T cellsImmune cell infiltrationCOX-2 expressionSmall intestinal tumorigenesisIL-17IL-17AIL-17A.IL-17F.Thymic atrophyIL-1βCell infiltrationT cellsGut homeostasisSmall intestineMiceSignificant decreaseC expressionTumorigenesisPropriaIntestineAblation
2010
Ablation of IL-17A abrogates progression of spontaneous intestinal tumorigenesis
Chae WJ, Gibson TF, Zelterman D, Hao L, Henegariu O, Bothwell AL. Ablation of IL-17A abrogates progression of spontaneous intestinal tumorigenesis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 5540-5544. PMID: 20212110, PMCID: PMC2851824, DOI: 10.1073/pnas.0912675107.Peer-Reviewed Original ResearchConceptsCD4 T cellsSpontaneous intestinal tumorigenesisIL-17AT cellsIntestinal tumorigenesisRegulatory T cell-mediated suppressionEffector CD4 T cellsT cell-mediated suppressionEndogenous IL-17ACell-mediated suppressionInfiltration of lymphocytesIntestinal epithelial cellsHyperproliferative potentialImmunological abnormalitiesAdoptive transferIL-10Proinflammatory mediatorsThymic atrophyInflammatory cytokinesImmunodeficient miceIntestinal architectureHeterozygote mutationsAltered functionMiceTumor development
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 ProteinsT-Lymphocytes, Helper-InducerTh1 CellsTh2 CellsTransforming 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
2006
Pivotal roles of CD8+ T cells restricted by MHC class I–like molecules in autoimmune diseases
Das G, Das J, Eynott P, Zhang Y, Bothwell AL, Van Kaer L, Shi Y. Pivotal roles of CD8+ T cells restricted by MHC class I–like molecules in autoimmune diseases. Journal Of Experimental Medicine 2006, 203: 2603-2611. PMID: 17088432, PMCID: PMC2118151, DOI: 10.1084/jem.20060936.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoimmune DiseasesBeta 2-MicroglobulinCD8-Positive T-LymphocytesCell SurvivalFemaleH-2 AntigensHistocompatibility Antigen H-2DHistocompatibility Antigens Class IIInflammatory Bowel DiseasesIslets of LangerhansLymphoproliferative DisordersMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNuclear ProteinsTrans-ActivatorsConceptsInnate-like lymphocytesInflammatory bowel diseaseMHC class IT cellsAutoimmune diseasesClass IMajor histocompatibility complex class IaLike moleculesClass II moleculesAdoptive transferBowel diseaseAutoimmune disordersLymphoproliferative syndromeImmunoregulatory functionsAdaptive immunityCD8Class IaDiseaseMiceInsulitisAutoimmunityPivotal roleCellsLymphocytesSyndrome
2004
Pax5-Deficient Mice Exhibit Early Onset Osteopenia with Increased Osteoclast Progenitors
Horowitz MC, Xi Y, Pflugh DL, Hesslein DG, Schatz DG, Lorenzo JA, Bothwell AL. Pax5-Deficient Mice Exhibit Early Onset Osteopenia with Increased Osteoclast Progenitors. The Journal Of Immunology 2004, 173: 6583-6591. PMID: 15557148, DOI: 10.4049/jimmunol.173.11.6583.Peer-Reviewed Original ResearchConceptsNumber of osteoclastsSpleen cellsB cellsOsteoclast developmentB cell-deficient miceCell-deficient miceControl spleen cellsB lymphocyte lineage cellsBone marrow cellsB-cell lineagePro-B cell stageMonocyte phenotypeBone massOsteoclast precursorsMice exhibitOsteoclast progenitorsMarrow cellsGrowth factorMiceOsteoclastsLineage cellsOsteopeniaCell lineagesCellsAdherent cells
2003
Immunopathology of human T cell responses to skin, artery and endothelial cell grafts in the human peripheral blood lymphocyte/severe combined immunodeficient mouse
Pober JS, Bothwell AL, Lorber MI, McNiff JM, Schechner JS, Tellides G. Immunopathology of human T cell responses to skin, artery and endothelial cell grafts in the human peripheral blood lymphocyte/severe combined immunodeficient mouse. Seminars In Immunopathology 2003, 25: 167-180. PMID: 12955465, DOI: 10.1007/s00281-003-0135-1.Peer-Reviewed Original ResearchConceptsLymphocytes/Peripheral blood lymphocyte/Human T cell responsesEndothelial cellsT cell responsesHuman peripheral bloodPig endotheliumHuman endothelial cellsPeripheral bloodCell graftsImmunodeficiency miceImmunodeficient miceCell responsesEndothelial liningRejection responseHuman vesselsBlood vesselsHuman arteriesLimited experienceTransplantationArteryImmunological propertiesSkinMiceHuman skin