0000000000481587

AUTHOR

Duong Anh Thuy Pham

showing 4 related works from this author

NFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network

2011

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

T-LymphocytesImmunologyNaive B cellB-cell receptorReceptors Antigen B-CellLymphocyte ActivationArticleMice03 medical and health sciences0302 clinical medicinemedicineAnimalsImmunology and AllergyB cell030304 developmental biologyB-Lymphocytes0303 health sciencesCD40NFATC Transcription Factorsintegumentary systembiologyCalcineurinCD22Germinal centerImmunoglobulin Class SwitchingMolecular biology3. Good healthB-1 cellCalcineurinmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinCalciumSpleenSignal TransductionJournal of Experimental Medicine
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NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells

2016

Epicutaneous application of Aldara cream containing the TLR7 agonist imiquimod (IMQ) to mice induces skin inflammation that exhibits many aspects of psoriasis, an inflammatory human skin disease. Here we show that mice depleted of B cells or bearing interleukin (IL)-10-deficient B cells show a fulminant inflammation upon IMQ exposure, whereas ablation of NFATc1 in B cells results in a suppression of Aldara-induced inflammation. In vitro, IMQ induces the proliferation and IL-10 expression by B cells that is blocked by BCR signals inducing NFATc1. By binding to HDAC1, a transcriptional repressor, and to an intronic site of the Il10 gene, NFATc1 suppresses IL-10 expression that dampens the pro…

0301 basic medicineNecrosisScienceGeneral Physics and AstronomyInflammationHuman skinImiquimodBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesPsoriasismedicineddc:610Multidisciplinaryintegumentary systemQInterleukinGeneral ChemistryTLR7medicine.diseaseInterleukin 10030104 developmental biologyImmunologyCancer researchmedicine.symptommedicine.drugNature Communications
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NFATc1 Induction in Peripheral T and B Lymphocytes

2013

Abstract NFAT transcription factors control the proliferation and survival of peripheral lymphocytes. We have reported previously that the short isoform NFATc1/αA whose generation is induced by immune receptor stimulation supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cells. We will show in this study that in novel bacterial artificial chromosome transgenic mice that express EGFP under the control of entire Nfatc1 locus the Nfatc1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripheral T and B cells. Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated in B, Th1, and Th2 cells, but…

LipopolysaccharidesGene isoformChromosomes Artificial BacterialProgrammed cell deathTransgeneGreen Fluorescent ProteinsImmunologyGene ExpressionMice TransgenicStimulationImmune receptorBiologyLymphocyte ActivationT-Lymphocytes RegulatoryAntibodiesMiceTh2 CellsGenes ReporterTransforming Growth Factor betaAnimalsProtein IsoformsImmunology and AllergyPromoter Regions GeneticTranscription factorCell ProliferationB-LymphocytesNFATC Transcription Factorsintegumentary systemNF-kappa BCD28NFATTh1 CellsMolecular biologyMice Inbred C57BLTh17 CellsThe Journal of Immunology
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NF-κB factors control the induction of NFATc1 in B lymphocytes

2014

In peripheral lymphocytes, the transcription factors (TFs) NF-κB, NFAT, and AP-1 are the prime targets of signals that emerge from immune receptors. Upon activation, these TFs induce gene networks that orchestrate the growth, expansion, and effector function of peripheral lymphocytes. NFAT and NF-κB factors share several properties, such as a similar mode of induction and architecture in their DNA-binding domain, and there is a subgroup of κB-like DNA promoter motifs that are bound by both types of TFs. However, unlike NFAT and AP-1 factors that interact and collaborate in binding to DNA, NFAT, and NF-κB seem neither to interact nor to collaborate. We show here that NF-κB1/p50 and c-Rel, th…

Gene isoformintegumentary systemEffectorImmunologybreakpoint cluster regionNFATNF-κBBiologyChromatinCell biologychemistry.chemical_compoundchemistryCancer researchImmunology and AllergyReceptorTranscription factorEuropean Journal of Immunology
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