2015
IL-21 Promotes Pulmonary Fibrosis through the Induction of Profibrotic CD8+ T Cells
Brodeur TY, Robidoux TE, Weinstein JS, Craft J, Swain SL, Marshak-Rothstein A. IL-21 Promotes Pulmonary Fibrosis through the Induction of Profibrotic CD8+ T Cells. The Journal Of Immunology 2015, 195: 5251-5260. PMID: 26519529, PMCID: PMC4655158, DOI: 10.4049/jimmunol.1500777.Peer-Reviewed Original ResearchLocal Triggering of the ICOS Coreceptor by CD11c+ Myeloid Cells Drives Organ Inflammation in Lupus
Teichmann LL, Cullen JL, Kashgarian M, Dong C, Craft J, Shlomchik MJ. Local Triggering of the ICOS Coreceptor by CD11c+ Myeloid Cells Drives Organ Inflammation in Lupus. Immunity 2015, 42: 552-565. PMID: 25786178, PMCID: PMC4456685, DOI: 10.1016/j.immuni.2015.02.015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAutoantibodiesCD11c AntigenCell DifferentiationFemaleGene Expression RegulationHumansInducible T-Cell Co-Stimulator LigandInducible T-Cell Co-Stimulator ProteinKidneyLungLupus NephritisMice, TransgenicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionT-Lymphocytes, Helper-InducerConceptsInducible T-cell costimulatorOrgan inflammationICOS ligandFollicular helper cell differentiationLupus-prone MRLT-cell costimulatorHelper cell differentiationLupus pathologyLung inflammationAutoantibody formationAutoantibody productionMurine lupusInflamed organsLymphoid tissueT cellsB cellsPathogenic relevanceInflammationLupusPI3K-AktSelective ablationCell differentiationNonredundant rolePotent promoterCells
2011
The Growth Factor Progranulin Binds to TNF Receptors and Is Therapeutic Against Inflammatory Arthritis in Mice
Tang W, Lu Y, Tian QY, Zhang Y, Guo FJ, Liu GY, Syed NM, Lai Y, Lin EA, Kong L, Su J, Yin F, Ding AH, Zanin-Zhorov A, Dustin ML, Tao J, Craft J, Yin Z, Feng JQ, Abramson SB, Yu XP, Liu CJ. The Growth Factor Progranulin Binds to TNF Receptors and Is Therapeutic Against Inflammatory Arthritis in Mice. Science 2011, 332: 478-484. PMID: 21393509, PMCID: PMC3104397, DOI: 10.1126/science.1199214.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAnimalsAnti-Inflammatory Agents, Non-SteroidalArthritis, ExperimentalCartilage, ArticularFemaleGranulinsHumansIntercellular Signaling Peptides and ProteinsLigandsMaleMiceMice, Inbred StrainsMice, KnockoutMice, TransgenicMiddle AgedProgranulinsProtein Interaction Domains and MotifsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRecombinant Fusion ProteinsRecombinant ProteinsSignal TransductionT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaYoung AdultConceptsInflammatory arthritisAdministration of progranulinAntagonist of TNFαCollagen-induced arthritisArthritis mouse modelPGRN-deficient miceNew potential therapeutic interventionsPotential therapeutic interventionsGrowth factor progranulinNecrosis factor receptorRheumatoid arthritisMouse modelArthritisTherapeutic interventionsProgranulinTNF receptorFactor receptorMiceReceptorsInflammationTissue repairTNFαIntracellular signalingAtsttrinTNFRDissecting the Immune Cell Mayhem That Drives Lupus Pathogenesis
Craft JE. Dissecting the Immune Cell Mayhem That Drives Lupus Pathogenesis. Science Translational Medicine 2011, 3: 73ps9. PMID: 21389262, PMCID: PMC3694130, DOI: 10.1126/scitranslmed.3002138.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusPathogenesis of SLEAutoimmune disease systemic lupus erythematosusDisease systemic lupus erythematosusSerious side effectsScience Translational MedicineLupus pathogenesisLupus erythematosusImmunosuppressive drugsCombination therapyCommon treatmentSide effectsImmune systemPathogenesisTherapyTranslational medicineErythematosusInflammationInterferonNeutrophils
2009
Thymic self-reactivity selects natural interleukin 17–producing T cells that can regulate peripheral inflammation
Marks BR, Nowyhed HN, Choi JY, Poholek AC, Odegard JM, Flavell RA, Craft J. Thymic self-reactivity selects natural interleukin 17–producing T cells that can regulate peripheral inflammation. Nature Immunology 2009, 10: 1125-1132. PMID: 19734905, PMCID: PMC2751862, DOI: 10.1038/ni.1783.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoantigensCD4-Positive T-LymphocytesCell DifferentiationEnzyme-Linked Immunosorbent AssayFlow CytometryInflammationIntegrin alpha4beta1Interleukin-17Interleukin-23Interleukin-6InterleukinsMiceMice, TransgenicNuclear Receptor Subfamily 1, Group F, Member 3Polymerase Chain ReactionReceptors, CCR6Receptors, Retinoic AcidReceptors, Thyroid HormoneThymus GlandT-Lymphocyte SubsetsTransforming Growth Factor beta
2002
Transgenic 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