Search results for "Transgenic"

showing 10 items of 552 documents

TCR V alpha chain expression influences reactivity to the hapten TNP.

1997

We have recently demonstrated a remarkable selection of in vitro cultivated, TNP-specific polyclonal T cell lines for the expression of a TCR beta chain encoded by the V beta 8.2 gene. The goal of the present study was to analyse V alpha usage in V beta 8.2 T cells responsive to TNP, using TNP-specific T cell lines derived from three common strains of mice, as well as from V beta 8.2 transgenic mice. Results indicate that in vitro TNP stimulation of T cells from TNP-immune mice results in significant skewing of V alpha usage among responding V beta 8.2+ T cells, with overexpression observed for V alpha 3.2 and V alpha 8. These results indicate that V alpha expression influences recognition …

T cellReceptors Antigen T-Cell alpha-betaT-LymphocytesImmunologychemical and pharmacologic phenomenaMice TransgenicLymphocyte ActivationEpitopesMiceAntigenmedicineImmunology and AllergyAnimalsAntibodies BlockingCells CulturedMice Inbred BALB Cbiologyorganic chemicalsT-cell receptorAntibodies Monoclonalhemic and immune systemsGeneral MedicineT lymphocyteMolecular biologyeye diseasesIn vitroMice Inbred C57BLmedicine.anatomical_structurePolyclonal antibodiesMultigene FamilyTrinitrobenzenesbiology.proteinMice Inbred CBALymph NodestissuesHaptenHaptensAlpha chainInternational immunology
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Intrahepatic myeloid-cell aggregates enable local proliferation of CD8+T cells and successful immunotherapy against chronic viral liver infection

2013

Chronic infection is difficult to overcome because of exhaustion or depletion of cytotoxic effector CD8(+) T cells (cytotoxic T lymphoytes (CTLs)). Here we report that signaling via Toll-like receptors (TLRs) induced intrahepatic aggregates of myeloid cells that enabled the population expansion of CTLs (iMATEs: 'intrahepatic myeloid-cell aggregates for T cell population expansion') without causing immunopathology. In the liver, CTL proliferation was restricted to iMATEs that were composed of inflammatory monocyte-derived CD11b(+) cells. Signaling via tumor-necrosis factor (TNF) caused iMATE formation that facilitated costimulation dependent on the receptor OX40 for expansion of the CTL popu…

T cellmedicine.medical_treatmentImmunologyPopulationGreen Fluorescent ProteinsMice TransgenicBiologyCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisMicemedicineImmunology and AllergyCytotoxic T cellAnimalsLymphocytic choriomeningitis virusMyeloid CellseducationCell ProliferationMice Knockouteducation.field_of_studyLiver infectionCD11b AntigenMicroscopy ConfocalLiver DiseasesImmunotherapyReceptors OX40Flow CytometryMice Inbred C57BLCTL*Chronic infectionmedicine.anatomical_structureAnimals NewbornLiverToll-Like Receptor 9ImmunologyChronic DiseaseHost-Pathogen InteractionsImmunotherapyCD8Signal TransductionT-Lymphocytes CytotoxicNature Immunology
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Susceptibility to collagen-induced arthritis is modulated by TGFβ responsiveness of T cells

2004

The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice t…

T-LymphocytesMice Inbred StrainsMice Transgenictransgenic miceTh1 CellsArthritis ExperimentalSeverity of Illness Indexdominant negative TGFβ type II receptorArthritis RheumatoidMiceMice Inbred DBATransforming Growth Factor betaAnimalsCytokinesCattleDisease SusceptibilityLymph NodesCollagen Type IICells CulturedCrosses GeneticResearch ArticleIFNγCell ProliferationArthritis Research & Therapy
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Tolerance without clonal expansion: self-antigen-expressing B cells program self-reactive T cells for future deletion.

2008

Abstract B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by abl…

T-LymphocytesProgrammed Cell Death 1 ReceptorAutoimmunityAntigens CD/biosynthesisAntigens CD5/geneticsAutoantigensInterleukin 21MiceImmunology and AllergyCytotoxic T cellHomeostasisCTLA-4 AntigenIL-2 receptorAntigens Differentiation/biosynthesisB-LymphocytesAntigens CD/geneticsB-Lymphocytes/immunologyT-Lymphocytes/metabolismNatural killer T cellCell biologymedicine.anatomical_structureHomeostasis/immunology2723 Immunology and AllergyAntigens CD5/biosynthesisAntigens Differentiation/geneticsAntigens CD5/immunologyT cellImmunologyAntigens CD/immunologyClonal Deletion610 Medicine & healthchemical and pharmacologic phenomenaMice TransgenicBiologyAutoantigens/biosynthesisCD5 AntigensAutoimmunity/physiologyAutoantigens/immunologyAntigens CDmedicineAnimalsB-Lymphocytes/metabolismAntigen-presenting cellCell Proliferation2403 ImmunologyAntigens Differentiation/immunologyGene Expression Regulation/immunologyCD40Clonal Deletion/physiologyT-Lymphocytes/immunologyAntigens Differentiation10040 Clinic for NeurologyB-1 cellGene Expression Regulationbiology.protein
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Cutting Edge: IL-23 Cross-Regulates IL-12 Production in T Cell-Dependent Experimental Colitis

2006

Abstract Although IL-12 and IL-23 share the common p40 subunit, IL-23, rather than IL-12, seems to drive the pathogenesis of experimental autoimmune encephalomyelitis and arthritis, because IL-23/p19 knockout mice are protected from disease. In contrast, we describe in this study that newly created LacZ knockin mice deficient for IL-23 p19 were highly susceptible for the development of experimental T cell-mediated TNBS colitis and showed even more severe colitis than wild-type mice by endoscopic and histologic criteria. Subsequent studies revealed that dendritic cells from p19-deficient mice produce elevated levels of IL-12, and that IL-23 down-regulates IL-12 expression upon TLR ligation. …

T-LymphocytesTransgeneT cellImmunologyDown-RegulationMice TransgenicInterleukin-23PathogenesisMiceInterleukin 23AnimalsImmunology and AllergyMedicineColitisCells Culturedbusiness.industryInterleukinsExperimental autoimmune encephalomyelitisColitismedicine.diseaseInterleukin-12Survival RateDisease Models AnimalProtein Subunitsmedicine.anatomical_structureImmunologyKnockout mouseInterleukin-23 Subunit p19Interleukin 12Disease SusceptibilitybusinessThe Journal of Immunology
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T Cells Integrate Local and Global Cues to Discriminate between Structurally Similar Antigens

2015

International audience; T lymphocytes' ability to discriminate between structurally related antigens has been attributed to the unique signaling properties of the T cell receptor. However, recent studies have suggested that the output of this discrimination process is conditioned by environmental cues. Here, we demonstrate how the IL-2 cytokine, collectively generated by strongly activated T cell clones, can induce weaker T cell clones to proliferate. We identify the PI3K pathway as being critical for integrating the antigen and cytokine responses and for controlling cell-cycle entry. We build a hybrid stochastic/deterministic computational model that accounts for such signal synergism and …

T-Lymphocytesmedicine.medical_treatmentT cellEFFECTORMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyLYMPHOCYTESArticleGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineACTIVATIONMicePhosphatidylinositol 3-KinasesAntigenmedicineAnimalsAntigenslcsh:QH301-705.5Sensory cuePI3K/AKT/mTOR pathwayAFFINITYIL-2T-cell receptorMEMORYPROLIFERATIONRECOGNITIONCell biologyMice Inbred C57BLCytokinemedicine.anatomical_structureDIFFERENTIATIONlcsh:Biology (General)ImmunologyCytokinesInterleukin-2Signal transductionTCRSignal Transduction
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Defective Postnatal Neurogenesis and Disorganization of the Rostral Migratory Stream in Absence of theVax1Homeobox Gene

2004

The subventricular zone (SVZ) is one of the sources of adult neural stem cells (ANSCs) in the mouse brain. Precursor cells proliferate in the SVZ and migrate through the rostral migratory stream (RMS) to the olfactory bulb (OB), where they differentiate into granule and periglomerular cells. Few transcription factors are known to be responsible for regulating NSC proliferation, migration, and differentiation processes; even fewer have been found to be responsible for the organization of the SVZ and RMS. For this reason, we studied the ventral anterior homeobox (Vax1) gene in NSC proliferation and in SVZ organization. We found thatVax1is strongly expressed in the SVZ and in the RMS and that,…

TelencephalonRostral migratory streamanimal diseasesCellular differentiationDevelopment/Plasticity/RepairSubventricular zoneMice TransgenicNerve Tissue ProteinsBiologyMiceCell MovementPrecursor cellmedicineAnimalsCell ProliferationHomeodomain ProteinsMice KnockoutStem CellsGeneral NeuroscienceNeuropeptidesGenes HomeoboxGene Expression Regulation DevelopmentalCell DifferentiationOlfactory BulbNeural stem cellOlfactory bulbDNA-Binding Proteinsmedicine.anatomical_structurenervous systemStem cellEpendymaNeuroscienceTranscription FactorsThe Journal of Neuroscience
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Dimerization of visinin-like protein 1 is regulated by oxidative stress and calcium and is a pathological hallmark of amyotrophic lateral sclerosis

2014

AbstractRedox control of proteins that form disulfide bonds upon oxidative challenge is an emerging topic in the physiological and pathophysiological regulation of protein function. We have investigated the role of the neuronal calcium sensor protein visinin-like protein 1 (VILIP-1) as a novel redox sensor in a cellular system. We have found oxidative stress to trigger dimerization of VILIP-1 within a cellular environment and identified thioredoxin reductase as responsible for facilitating the remonomerization of the dimeric protein. Dimerization is modulated by calcium and not dependent on the myristoylation of VILIP-1. Furthermore, we show by site-directed mutagenesis that dimerization is…

Thioredoxin reductaseAmino Acid MotifsBlotting Westernchemistry.chemical_elementMice TransgenicFree radicalsOxidative phosphorylationCalciumProtein aggregationmedicine.disease_causeBiochemistryMass SpectrometryMicechemistry.chemical_compoundSuperoxide Dismutase-1BAPTAPhysiology (medical)VILIP-1medicineAnimalsHumansCysteineMyristoylationSuperoxide DismutaseChemistryHEK 293 cellsAmyotrophic lateral sclerosisRedox sensorImmunohistochemistryCell biologyDisease Models AnimalOxidative StressHEK293 CellsBiochemistryNeurocalcinMutagenesis Site-DirectedCalciumProtein MultimerizationOxidation-ReductionOxidative stressFree Radical Biology and Medicine
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Profilin1 regulates sternum development and endochondral bone formation.

2012

Bone development is a dynamic process that requires cell motility and morphological adaptation under the control of actin cytoskeleton. This actin cytoskeleton system is regulated by critical modulators including actin-binding proteins. Among them, profilin1 (Pfn1) is a key player to control actin fiber structure, and it is involved in a number of cellular activities such as migration. During the early phase of body development, skeletal stem cells and osteoblastic progenitor cells migrate to form initial rudiments for future skeletons. During this migration, these cells extend their process based on actin cytoskeletal rearrangement to locate themselves in an appropriate location within mic…

Time FactorsGenotypeMice Transgenicmacromolecular substancesBiologyTransfectionBiochemistryBone and BonesMiceProfilinsCell MovementOsteogenesisBone cellAnimalsProgenitor cellRNA Small InterferingCytoskeletonMolecular BiologyActinAllelesCytoskeletonMice KnockoutOsteoblastsMesenchymal stem cellGene Expression Regulation DevelopmentalCell migrationMesenchymal Stem CellsCell BiologyX-Ray MicrotomographyActin cytoskeletonCell biologyCartilageImmunologyNIH 3T3 CellsStem cellDevelopmental BiologyThe Journal of biological chemistry
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Cross-circulation and Cell Distribution Kinetics in Parabiotic Mice

2011

Blood-borne nucleated cells participate not only in inflammation, but in tissue repair and regeneration. Because progenitor and stem cell populations have a low concentration in the blood, the circulation kinetics and tissue distribution of these cells is largely unknown. An important approach to tracking cell lineage is the use of fluorescent tracers and parabiotic models of cross-circulation. Here, we investigated the cross-circulation and cell distribution kinetics of C57/B6 GFP(+)/wild-type parabionts. Flow cytometry analysis of the peripheral blood after parabiosis demonstrated no evidence for a "parabiotic barrier" based on cell size or surface characterstics; all peripheral blood cel…

Time FactorsPhysiologyParabiosisT-LymphocytesClinical BiochemistryGreen Fluorescent ProteinsParabiosisMice TransgenicBiologyArticleFlow cytometryMiceNucleated cellWeight LossmedicineAnimalsPeripheral blood cellWhole bloodmedicine.diagnostic_testBehavior AnimalCell BiologyMolecular biologyMice Inbred C57BLLymphatic systemGene Expression RegulationImmunologyLymphStem cell
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