2021
Type I Interferon–Activated STAT4 Regulation of Follicular Helper T Cell–Dependent Cytokine and Immunoglobulin Production in Lupus
Dong X, Antao OQ, Song W, Sanchez GM, Zembrzuski K, Koumpouras F, Lemenze A, Craft J, Weinstein JS. Type I Interferon–Activated STAT4 Regulation of Follicular Helper T Cell–Dependent Cytokine and Immunoglobulin Production in Lupus. Arthritis & Rheumatology 2021, 73: 478-489. PMID: 33512094, PMCID: PMC7914134, DOI: 10.1002/art.41532.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntibody FormationAutoantibodiesB-LymphocytesCase-Control StudiesCytokinesDisease Models, AnimalFemaleHumansImmunoglobulinsInterferon Type IInterferon-gammaInterleukinsLupus Erythematosus, SystemicMaleMice, Inbred MRL lprMiddle AgedRNA-SeqSTAT4 Transcription FactorT Follicular Helper CellsConceptsSystemic lupus erythematosusTfh-like cellsTfh cellsIL-21Human lupusDisease activityCytokine productionSTAT4 activationImmunoglobulin productionPathogenic B cell responsesCourse of lupusClinical disease activityT cell secretionLupus-prone miceHealthy control subjectsCourse of diseaseB cell responsesCytokine interleukin-21Potential therapeutic targetType I IFNB cell maturationSLE patientsPathogenic cytokinesLupus erythematosusInterleukin-21
2017
STAT4 and T-bet control follicular helper T cell development in viral infections
Weinstein JS, Laidlaw BJ, Lu Y, Wang JK, Schulz VP, Li N, Herman EI, Kaech SM, Gallagher PG, Craft J. STAT4 and T-bet control follicular helper T cell development in viral infections. Journal Of Experimental Medicine 2017, 215: 337-355. PMID: 29212666, PMCID: PMC5748849, DOI: 10.1084/jem.20170457.Peer-Reviewed Original ResearchConceptsIL-21Tfh cellsT-betViral infectionFollicular helper T cellsHelper T cell developmentAcute viral infectionIFN-γ productionHelper T cellsGerminal center B cell survivalB cell survivalT cell developmentIL-4Viral challengeIL-9T cellsImmunoglobulin isotypesIFNSoluble factorsGC responseInfectionGC reactionSTAT4BCL6Cell survival
2000
Dominance of IL-12 Over IL-4 in γδ T Cell Differentiation Leads to Default Production of IFN-γ: Failure to Down-Regulate IL-12 Receptor β2-Chain Expression
Yin Z, Zhang D, Welte T, Bahtiyar G, Jung S, Liu L, Fu X, Ray A, Craft J. Dominance of IL-12 Over IL-4 in γδ T Cell Differentiation Leads to Default Production of IFN-γ: Failure to Down-Regulate IL-12 Receptor β2-Chain Expression. The Journal Of Immunology 2000, 164: 3056-3064. PMID: 10706694, DOI: 10.4049/jimmunol.164.6.3056.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCells, CulturedCytokinesDNA-Binding ProteinsDown-RegulationGATA3 Transcription FactorInterferon-gammaInterleukin-12Interleukin-4Lymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, Antigen, T-Cell, gamma-deltaReceptors, InterleukinReceptors, Interleukin-12Signal TransductionSTAT3 Transcription FactorSTAT4 Transcription FactorTh1 CellsTh2 CellsT-Lymphocyte SubsetsTrans-ActivatorsConceptsGamma delta T cellsDelta T cellsT cellsIFN-gammaIL-12IL-4Murine gamma delta T cellsSplenic gamma delta T cellsAlpha beta T cellsIFN-gamma-producing cellsΓδ T-cell differentiationIL-4-secreting cellsBeta T cellsTh2-like cytokinesIL-12 receptorTranscription factor GATA-3T cell differentiationTumor immunityTh1 cellsTh2 cellsSuch cytokinesFinding independentReceptor betaGATA-3Intracellular pathogens