2024
The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response
Even Z, Meli A, Tyagi A, Vidyarthi A, Briggs N, de Kouchkovsky D, Kong Y, Wang Y, Waizman D, Rice T, De Kumar B, Wang X, Palm N, Craft J, Basu M, Ghosh S, Rothlin C. The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response. Immunity 2024, 57: 1893-1907.e6. PMID: 39096910, PMCID: PMC11421571, DOI: 10.1016/j.immuni.2024.07.006.Peer-Reviewed Original ResearchT cell receptorImmune responseNaive CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cellsIFN-IHelminth infectionsNippostrongylus brasiliensis infectionDecreased immune responseType I interferonNaive TT cellsMemory-likeUnrelated antigensTranscriptional changesExtracellular matrixSPF miceCell receptorsI interferonGerm-freeResponse to certain environmental cuesInfectionMiceFunctional changesCell transcriptional statesTranscriptional heterogeneity
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
Identification of a T follicular helper cell subset that drives anaphylactic IgE
Gowthaman U, Chen JS, Zhang B, Flynn WF, Lu Y, Song W, Joseph J, Gertie JA, Xu L, Collet MA, Grassmann JDS, Simoneau T, Chiang D, Berin MC, Craft JE, Weinstein JS, Williams A, Eisenbarth SC. Identification of a T follicular helper cell subset that drives anaphylactic IgE. Science 2019, 365 PMID: 31371561, PMCID: PMC6901029, DOI: 10.1126/science.aaw6433.Peer-Reviewed Original ResearchConceptsInterleukin-4B cellsFollicular Helper Cell SubsetsLow-affinity IgEFollicular helper cellsAllergen-specific IgEHelper cell subsetsIsotypes of antibodiesAlternative therapeutic targetsTranscription factor Bcl6Anaphylactic IgECytokine profileIgE productionCell subsetsHelper cellsImmunoglobulin ETherapeutic targetIgEAnaphylaxisAllergensCellular mechanismsRare populationCellsMiceGATA3
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 Research
2014
Transcription factor Ascl2 limits Tfh cell differentiation and function (IRC8P.493)
Bertino S, Dong X, Laidlaw B, Craft J. Transcription factor Ascl2 limits Tfh cell differentiation and function (IRC8P.493). The Journal Of Immunology 2014, 192: 190.21-190.21. DOI: 10.4049/jimmunol.192.supp.190.21.Peer-Reviewed Original ResearchTfh cellsIL-4T cellsAntibody productionCD4 T cell compartmentFollicular helper T cellsTfh cell subsetsTfh cell differentiationTfh cell developmentIL-4 productionT cell compartmentHelper T cellsLarge germinal centersGerminal center responseSecretion of cytokinesGerminal center formationB cell maturationGC B cellsIL-21Germinal centersB cellsCenter responseCell maturationConditional deletionMice
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
2009
Lupus immunotherapy using CD4 targeted nanoparticles (48.29)
Look M, Stern E, Wang Q, DiPlacido L, Craft J, Fahmy T. Lupus immunotherapy using CD4 targeted nanoparticles (48.29). The Journal Of Immunology 2009, 182: 48.29-48.29. DOI: 10.4049/jimmunol.182.supp.48.29.Peer-Reviewed Original ResearchNZB/W F1 miceW F1 miceCD4 T cellsImmunosuppressive drugsDisease progressionF1 miceT cellsImmunosuppressive drug dosageSystemic lupus erythematosusNanoparticle therapyConventional therapeutic regimensFrequency of dosageLupus erythematosusAutoantibody productionTherapeutic regimensWeekly treatmentTherapeutic featuresAnimal modelsB cellsDrug dosageTherapeutic efficacyLupusImmunotherapyTherapyMice
2007
CNS lupus in MRL/Faslpr mice (130.15)
Choi J, Chahboune H, Hyder F, Craft J. CNS lupus in MRL/Faslpr mice (130.15). The Journal Of Immunology 2007, 178: s230-s230. DOI: 10.4049/jimmunol.178.supp.130.15.Peer-Reviewed Original ResearchMRL/Faslpr miceFaslpr miceDiffusion tensor imagingControl miceStructural abnormalitiesCentral nervous system injurySpontaneous autoimmune diseaseLupus-prone miceNervous system injuryToll-like receptorsWeeks of ageCNS lupusIg depositionNeurological deficitsHuman SLENeuropsychiatric involvementSystem injuryAntibody depositionAutoimmune diseasesDTI alterationsMRL miceChoroid plexusMiceTensor imagingHippocampus
2006
γδ T Cells Facilitate Adaptive Immunity against West Nile Virus Infection in Mice
Wang T, Gao Y, Scully E, Davis CT, Anderson JF, Welte T, Ledizet M, Koski R, Madri JA, Barrett A, Yin Z, Craft J, Fikrig E. γδ T Cells Facilitate Adaptive Immunity against West Nile Virus Infection in Mice. The Journal Of Immunology 2006, 177: 1825-1832. PMID: 16849493, DOI: 10.4049/jimmunol.177.3.1825.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsCD8-Positive T-LymphocytesGenetic Predisposition to DiseaseImmunity, CellularImmunity, InnateImmunization, SecondaryImmunoglobulin GImmunoglobulin MImmunologic MemoryLymphocyte DepletionMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-Cell, gamma-deltaRecurrenceT-Lymphocyte SubsetsWest Nile FeverWest Nile virusConceptsGammadelta T cellsWild-type miceT cellsWN virus infectionPrimary infectionVirus infectionWN virusNaive miceSecondary challengeImmune responseAdaptive immunityCD8 memory T cellsWest Nile virus infectionMemory T cellsProtective immune responseAdaptive immune responsesAdoptive transferWest Nile virusAb responsesLethal infectionViral challengeFatal meningoencephalitisSecondary infectionInfectionMice
2004
Resistance to Development of Collagen-Induced Arthritis in C57BL/6 Mice Is Due to a Defect in Secondary, but Not in Primary, Immune Response
Pan M, Kang I, Craft J, Yin Z. Resistance to Development of Collagen-Induced Arthritis in C57BL/6 Mice Is Due to a Defect in Secondary, but Not in Primary, Immune Response. Journal Of Clinical Immunology 2004, 24: 481-491. PMID: 15359107, DOI: 10.1023/b:joci.0000040919.16739.44.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisB6 miceImmune responseSimilar T cell proliferationBovine type II collagenB cell immune responsesH-2b backgroundAnti-CII antibodiesHuman rheumatoid arthritisT cell responsesCell immune responsesSecondary immune responseT cell proliferationCII AbsCytokine responsesRheumatoid arthritisInitial immunizationC57BL/6 miceRodent modelsArthritisType II collagenDay 14Cell responsesDay 12Mice
2003
Age-dependent Requirement for γδ T Cells in the Primary but Not Secondary Protective Immune Response against an Intestinal Parasite
Ramsburg E, Tigelaar R, Craft J, Hayday A. Age-dependent Requirement for γδ T Cells in the Primary but Not Secondary Protective Immune Response against an Intestinal Parasite. Journal Of Experimental Medicine 2003, 198: 1403-1414. PMID: 14597739, PMCID: PMC2194243, DOI: 10.1084/jem.20030050.Peer-Reviewed Original ResearchConceptsAlphabeta T cellsGammadelta cellsT cellsYoung miceImmune responseAdult miceIntestinal parasitesPathogen-specific immunityΓδ T cellsCellular immune responsesProtective immune responseT cell receptorWk of ageAdoptive transferDevelopment of resistanceImmune protectionNewborn recipientsEimeria vermiformisAge-dependent requirementsCell receptorMiceE. vermiformisLymphoid progenitorsInfectionYoung hostsRole of the H‐2 haplotype in Fas‐intact lupus‐prone MRL mice: association with autoantibodies but not renal disease
Kong PL, Zhu T, Madaio MP, Craft J. Role of the H‐2 haplotype in Fas‐intact lupus‐prone MRL mice: association with autoantibodies but not renal disease. Arthritis & Rheumatism 2003, 48: 2992-2995. PMID: 14558109, DOI: 10.1002/art.11308.Peer-Reviewed Original ResearchIFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection
Wang T, Scully E, Yin Z, Kim JH, Wang S, Yan J, Mamula M, Anderson JF, Craft J, Fikrig E. IFN-γ-Producing γδ T Cells Help Control Murine West Nile Virus Infection. The Journal Of Immunology 2003, 171: 2524-2531. PMID: 12928402, DOI: 10.4049/jimmunol.171.5.2524.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsBloodCell DivisionCells, CulturedCytotoxicity, ImmunologicEncephalitis, ViralFemaleGenes, T-Cell Receptor betaGenes, T-Cell Receptor deltaGenetic Predisposition to DiseaseInterferon-gammaLymphoid TissueMiceMice, Inbred C57BLMice, KnockoutReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaSeverity of Illness IndexT-Lymphocyte SubsetsViral LoadWest Nile FeverWest Nile virusConceptsGammadelta T cellsWN virus infectionT cellsVirus infectionIFN-gamma-producing gammadelta T cellsWest Nile virus infectionPrevention of mortalityΓδ T cellsSplenic T cellsWild-type miceEx vivo assaysAdoptive transferWest Nile virusPerforin expressionViral loadFatal meningoencephalitisIFN-gammaMiceInfectionWN virusNile virusVivo assaysLaboratory miceCellsVirusIntrinsic T Cell Defects in Systemic Autoimmunity
KONG PL, ODEGARD JM, BOUZAHZAH F, CHOI J, EARDLEY LD, ZIELINSKI CE, CRAFT JE. Intrinsic T Cell Defects in Systemic Autoimmunity. Annals Of The New York Academy Of Sciences 2003, 987: 60-67. PMID: 12727624, DOI: 10.1111/j.1749-6632.2003.tb06033.x.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusT cell defectsIntrinsic T cell defectCell defectsT cell toleranceLupus pathogenesisLupus erythematosusAutoimmune diseasesSystemic autoimmunityT cellsCell toleranceNuclear antigenGenetic causeLupusBiochemical natureErythematosusAutoimmunityPathogenesisAntigenDiseaseMice
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 mechanismsRegulation of T cell-dependent autoantibody production by a γδ T cell line derived from lupus-prone mice
Fujii T, Okada M, Craft J. Regulation of T cell-dependent autoantibody production by a γδ T cell line derived from lupus-prone mice. Cellular Immunology 2002, 217: 23-35. PMID: 12425998, DOI: 10.1016/s0008-8749(02)00509-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, AntinuclearApoptosisB-LymphocytesCell LineCoculture TechniquesCytotoxicity Tests, ImmunologicDNAInterleukin-10Lupus Erythematosus, SystemicLymphocyte ActivationLymphocyte CooperationMiceMice, Inbred C57BLMice, Inbred MRL lprMice, KnockoutReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaT-Lymphocytes, Helper-InducerTumor Necrosis Factor-alphaConceptsGammadelta T cell linesT cell linesAnti-dsDNA productionMRL/B cellsAutoantibody productionCell linesLupus-prone miceMRL/MpGammadelta T cellsT helper cell linesB cell collaborationActivated B cellsContact-dependent mannerAlphabeta TSevere lupusGammadelta TAutoantibody synthesisMurine lupusLupus-proneT cellsCell collaborationHelper cell lineMiceLupus
2000
Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies
Nagaraju K, Raben N, Loeffler L, Parker T, Rochon P, Lee E, Danning C, Wada R, Thompson C, Bahtiyar G, Craft J, van Huijsduijnen R, Plotz P. Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 9209-9214. PMID: 10922072, PMCID: PMC16847, DOI: 10.1073/pnas.97.16.9209.Peer-Reviewed Original ResearchConceptsMHC class IMyositis-specific autoantibodiesClass IAutoimmune diseasesSkeletal muscleHuman inflammatory myopathiesHuman myositisInflammatory myopathiesAutoimmune myositisImmunological featuresSpontaneous human diseaseYoung miceAutoantibodiesMuscle cellsNonspecific eventsDiseaseMiceMyositisMuscleCommon specificityHuman diseasesSpecific patternsSpecificityStimuliMyopathy
1999
Lessons from Knockout and Transgenic Lupus-Prone Mice
Peng S, Craft J. Lessons from Knockout and Transgenic Lupus-Prone Mice. Contemporary Immunology 1999, 152-166. DOI: 10.1007/978-1-59259-703-1_10.Peer-Reviewed Original ResearchLupus-prone miceSystemic lupus erythematosusNZB ×Disease manifestationsStudy of lupusLupus-like symptomsMRL/MpPathogenesis of lupusB cell toleranceLupus erythematosusImmune deficiencyT cellsImmune organsB cellsDisease pathogenesisImmune systemMurine systemMouse strainsMajority of knowledgeFunctional activityMiceGenetic alterationsLupusHuman disease pathogenesisPathogenesis
1998
Influence of antigen organization on the development of lupus autoantibodies
Fatenejad S, Bennett M, Moslehi J, Craft J. Influence of antigen organization on the development of lupus autoantibodies. Arthritis & Rheumatism 1998, 41: 603-612. PMID: 9550469, DOI: 10.1002/1529-0131(199804)41:4<603::aid-art7>3.0.co;2-e.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesAutoantibodiesAutoantigensGene ExpressionHeLa CellsHumansImmune ToleranceImmunizationLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, Inbred StrainsRecombinant Fusion ProteinsRecombinant ProteinsRibonucleoprotein, U1 Small NuclearRibonucleoproteins, Small NuclearRNA-Binding ProteinsT-LymphocytesTumor Cells, CulturedConceptsSystemic lupus erythematosusDevelopment of antibodiesH-2b backgroundDevelopment of lupusT cell responsesT cell toleranceAssessment of antibodiesNative snRNP particlesTypical immune responseLupus erythematosusAutoimmune responseNormal miceAntigen organizationImmune responseForeign immunogensH-2kCell toleranceMajor autoantigenCell responsesMiceRandom orderAntibodiesEukaryotic expression vectorLupusAutoantigens