2023
HIF-1 regulates pathogenic cytotoxic T cells in lupus skin disease
Little A, Chen P, Vesely M, Khan R, Fiedler J, Garritano J, Islam F, McNiff J, Craft J. HIF-1 regulates pathogenic cytotoxic T cells in lupus skin disease. JCI Insight 2023, 8: e166076. PMID: 37526979, PMCID: PMC10543720, DOI: 10.1172/jci.insight.166076.Peer-Reviewed Original ResearchConceptsCutaneous lupus erythematosusLupus skin diseaseT cellsSkin diseasesCytotoxic signatureInflammatory infiltrateHIF-1Tissue damageKidney-infiltrating T cellsSkin-infiltrating T cellsAutoimmune skin diseaseHIF-1 inhibitionSkin tissue damageLupus erythematosusSystemic diseaseTissue inflammationGranzyme BMouse modelInflammatory gene programDiseaseProtein levelsInfiltratesSkin environmentGene programPresent studyCutting Edge: IL-21 and Tissue-Specific Signals Instruct Tbet+CD11c+ B Cell Development following Viral Infection.
Song W, Sanchez G, Mayer D, Blackburn H, Chernova I, Flavell R, Weinstein J, Craft J. Cutting Edge: IL-21 and Tissue-Specific Signals Instruct Tbet+CD11c+ B Cell Development following Viral Infection. The Journal Of Immunology 2023, 210: 1861-1865. PMID: 37133336, PMCID: PMC10247523, DOI: 10.4049/jimmunol.2300027.Peer-Reviewed Original ResearchConceptsAge-associated B cellsIL-21Acute lymphocytic choriomeningitis virus infectionB cellsLymphocytic choriomeningitis virus infectionB cell activationHumoral immunityLymphoid organsVirus infectionMouse modelViral infectionB cell developmentCell activationLymphotoxin αVivo generationTissue-specific signalsInfectionDe novo generationOrgan contributionIFNTissue microenvironmentCell developmentLiverPivotal contributorStage-specific roles
2020
Repeat tick exposure elicits distinct immune responses in guinea pigs and mice
Kurokawa C, Narasimhan S, Vidyarthi A, Booth CJ, Mehta S, Meister L, Diktas H, Strank N, Lynn GE, DePonte K, Craft J, Fikrig E. Repeat tick exposure elicits distinct immune responses in guinea pigs and mice. Ticks And Tick-borne Diseases 2020, 11: 101529. PMID: 32993942, PMCID: PMC7530331, DOI: 10.1016/j.ttbdis.2020.101529.Peer-Reviewed Original ResearchConceptsGuinea pigsElicit distinct immune responsesDistinct immune responsesGuinea pig modelLocal blood flowImmune animalsInflammatory pathwaysTick rejectionMechanisms of resistanceImmune responseMouse modelVaccine candidatesBite siteBlood flowPig modelCoagulation pathwayComplement activationAcquired ResistanceProtective antigenTick detachmentTick proteinsBlood mealMiceTick infestationRNA sequencing
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
2012
Caspase‐activated DNase is required for maintenance of tolerance to lupus nuclear autoantigens
Jog NR, Frisoni L, Shi Q, Monestier M, Hernandez S, Craft J, Prak ET, Caricchio R. Caspase‐activated DNase is required for maintenance of tolerance to lupus nuclear autoantigens. Arthritis & Rheumatism 2012, 64: 1247-1256. PMID: 22127758, PMCID: PMC3292632, DOI: 10.1002/art.33448.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusAutoimmune responseMouse modelApoptotic cellsNuclear autoantigensDNA antibody titersLupus-prone miceAbsence of CADMaintenance of toleranceAutoreactive B cellsAnti-DNA antibodiesApoptotic modificationsLupus developmentGeneration of autoantigensAntinuclear antibodiesLupus erythematosusAntibody titersAutoimmune diseasesActive caspase-3Apoptotic bodiesB cellsMiceAutoantigensCAD deficiencyCaspase-3
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 signalingAtsttrinTNFR
2008
ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity
Odegard JM, Marks BR, DiPlacido LD, Poholek AC, Kono DH, Dong C, Flavell RA, Craft J. ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity. Journal Of Experimental Medicine 2008, 205: 2873-2886. PMID: 18981236, PMCID: PMC2585848, DOI: 10.1084/jem.20080840.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteAutoimmunityCell DifferentiationChemokinesDisease Models, AnimalGerminal CenterImmunoglobulin Class SwitchingImmunoglobulin GInducible T-Cell Co-Stimulator ProteinInterleukinsLupus Erythematosus, SystemicMembrane GlycoproteinsMiceMice, KnockoutPlasma CellsReceptors, CXCR4T-Lymphocyte SubsetsT-Lymphocytes, Helper-InducerConceptsEffector T cellsT cellsIL-21IgG productionCXC chemokine receptor 4 (CXCR4) expressionB cell helper functionFollicular helper T cellsChemokine receptor 4 expressionReceptor 4 expressionCD4 T cellsHelper T cellsMRL/MpJAutoimmune strainsP-selectin glycoprotein ligand-1Autoantibody productionChronic autoimmunitySystemic autoimmunityPlasma cellsExtrafollicular responseExtrafollicular sitesMouse modelGerminal centersHelper functionSelective lossLigand 1