2019
Impaired ATM activation in B cells is associated with bone resorption in rheumatoid arthritis
Mensah KA, Chen JW, Schickel JN, Isnardi I, Yamakawa N, Vega-Loza A, Anolik JH, Gatti RA, Gelfand EW, Montgomery RR, Horowitz MC, Craft JE, Meffre E. Impaired ATM activation in B cells is associated with bone resorption in rheumatoid arthritis. Science Translational Medicine 2019, 11 PMID: 31748230, PMCID: PMC7167286, DOI: 10.1126/scitranslmed.aaw4626.Peer-Reviewed Original ResearchConceptsRheumatoid arthritisB cellsHealthy donor controlsGroup of patientsHumanized mouse modelImmature B cellsGene segment usageErosive diseaseRA pathophysiologyBone erosionBone lossBone resorptionHigh prevalenceRANKL productionBone densityMouse modelReceptor activatorBone marrowPatientsDonor controlsCD21Segment usageArthritisElevated frequencyAtaxia telangiectasia
2005
Naive CD4+ T Cells from Lupus-Prone Fas-Intact MRL Mice Display TCR-Mediated Hyperproliferation Due to Intrinsic Threshold Defects in Activation
Zielinski CE, Jacob SN, Bouzahzah F, Ehrlich BE, Craft J. Naive CD4+ T Cells from Lupus-Prone Fas-Intact MRL Mice Display TCR-Mediated Hyperproliferation Due to Intrinsic Threshold Defects in Activation. The Journal Of Immunology 2005, 174: 5100-5109. PMID: 15814741, DOI: 10.4049/jimmunol.174.8.5100.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationAutoimmunityCalcium SignalingCD4-Positive T-LymphocytesCell ProliferationColumbidaeCytochromes cDendritic CellsFas ReceptorGenes, DominantInterleukin-2Lupus Erythematosus, SystemicLymphocyte ActivationMiceMice, Inbred MRL lprMice, Inbred StrainsMice, KnockoutMice, TransgenicPhenotypeReceptor-CD3 Complex, Antigen, T-CellReceptors, Antigen, T-CellSignal TransductionConceptsNaive CD4T cellsSelf-AgAutoreactive T cell activationMRL T cellsT cell toleranceF1 T cellsProximal defectsAnti-CD3 stimulationClass II MHCIL-2 productionT cell activationWild-type CD4Pigeon cytochrome cCell calcium signalingDendritic cellsControl miceMurine lupusObserved hyperactivityII MHCMRL miceIntracellular calciumLow thresholdPeptide AgCD4
2004
The Centromeric Region of Chromosome 7 from MRL Mice (Lmb3) Is an Epistatic Modifier of Fas for Autoimmune Disease Expression
Kong PL, Morel L, Croker BP, Craft J. The Centromeric Region of Chromosome 7 from MRL Mice (Lmb3) Is an Epistatic Modifier of Fas for Autoimmune Disease Expression. The Journal Of Immunology 2004, 172: 2785-2794. PMID: 14978078, DOI: 10.4049/jimmunol.172.5.2785.Peer-Reviewed Original ResearchConceptsMRL/Prototypic systemic autoimmune diseaseDouble-negative T cellsAutoimmune disease expressionEtiology of lupusResistant C57BL/6 backgroundLupus-prone miceSystemic autoimmune diseaseFas-deficient miceT cell activationLupus susceptibility lociAutoantibody productionAutoimmune diseasesKidney diseaseT cellsMRL miceAbsence of Fas
2002
IL-10 Regulates Murine Lupus
Yin Z, Bahtiyar G, Zhang N, Liu L, Zhu P, Robert ME, McNiff J, Madaio MP, Craft J. IL-10 Regulates Murine Lupus. The Journal Of Immunology 2002, 169: 2148-2155. PMID: 12165544, DOI: 10.4049/jimmunol.169.4.2148.Peer-Reviewed Original ResearchConceptsIL-10Murine lupusHuman systemic lupus erythematosusAnti-dsDNA autoantibody productionSeverity of lupusTh1 cytokine responseAnti-dsDNA autoantibodiesSystemic lupus erythematosusIFN-gamma productionIL-10 locusMRL/MpJPotential therapeutic benefitLupus syndromeSevere glomerulonephritisSevere lupusLupus modelsLupus erythematosusRIL-10Autoantibody productionCytokine responsesHuman lupusSerum concentrationsProtective effectSkin lesionsLittermate controlsTransgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*
Lee CG, Homer RJ, Cohn L, Link H, Jung S, Craft JE, Graham BS, Johnson TR, Elias JA. Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*. Journal Of Biological Chemistry 2002, 277: 35466-35474. PMID: 12107190, DOI: 10.1074/jbc.m206395200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceChloride ChannelsCloning, MolecularDNA PrimersFluorescent Antibody TechniqueGene Expression RegulationIn Situ HybridizationInflammationInterleukin-10Interleukin-13LungMiceMice, TransgenicMolecular Sequence DataMucoproteinsMucous MembranePhenotypePolymerase Chain ReactionReceptors, Interleukin-4STAT6 Transcription FactorTrans-ActivatorsConceptsMucus metaplasiaIL-10Tissue inflammationIL-13Tumor necrosis factor productionIL-13/ILLipopolysaccharide-induced inflammationNecrosis factor productionAirway fibrosisNeutrophil accumulationAirway remodelingSubepithelial fibrosisGob-5Levels of mRNAMetaplasiaInflammationTransgenic miceFibrosisSTAT-6Effector propertiesTransgenic overexpressionFactor productionMiceInterleukinMultiple mechanisms