Search results for "T CELLS"

showing 10 items of 498 documents

Mast Cell–deficient KitW-sh “Sash” Mutant Mice Display Aberrant Myelopoiesis Leading to the Accumulation of Splenocytes That Act as Myeloid-Derived S…

2013

Abstract Mast cell-deficient KitW-sh “sash” mice are widely used to investigate mast cell functions. However, mutations of c-Kit also affect additional cells of hematopoietic and nonimmune origin. In this study, we demonstrate that KitW-sh causes aberrant extramedullary myelopoiesis characterized by the expansion of immature lineage-negative cells, common myeloid progenitors, and granulocyte/macrophage progenitors in the spleen. A consistent feature shared by these cell types is the reduced expression of c-Kit. Populations expressing intermediate and high levels of Ly6G, a component of the myeloid differentiation Ag Gr-1, are also highly expanded in the spleen of sash mice. These cells are …

Cell typeMyeloidT cellImmunologyBiologyImmunophenotypingMice03 medical and health sciences0302 clinical medicineNeoplasmsmedicineAnimalsAntigens LyImmunology and AllergyMyeloid CellsMast CellsProgenitor cell030304 developmental biologyMice KnockoutMyelopoiesis0303 health sciencesCD11b AntigenMast cellAdoptive Transfer3. Good healthCell biologyProto-Oncogene Proteins c-kitHaematopoiesismedicine.anatomical_structureHematopoiesis ExtramedullaryMutationImmunologyMyeloid-derived Suppressor CellFemaleMyelopoiesisNeoplasm TransplantationSpleen030215 immunologyThe Journal of Immunology
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In Activated Murine Mast Cells, NFATc2 Is Critical for the Production of Autocrine IL-3, Thereby Promoting the Expression of IL-9

2019

Abstract IL-9 has lent its numerical designation to the Th9 subset of CD4+ Th cells, although it is also produced by additional cell types, including mast cells. It is a pleiotropic cytokine involved in allergic reactions, parasitic infections, autoimmune inflammation, and cancer immunity. In this article, we provide evidence that NFATc2 has contradictory functions in the expression of IL-9 in murine Th9 cells and bone marrow–derived mast cells (BMMC). The basis for this is our observation that the production of IL-9 in NFATc2-deficient Th9 cells is increased, whereas it is decreased in BMMC devoid of NFATc2. In addition, NFATc2 deficiency almost completely abrogates the expression of IL-3 …

Cell typeNFATC2medicine.medical_treatmentImmunologyCellAutocrine CommunicationMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyMast CellsAutocrine signallingCells CulturedSTAT5Feedback PhysiologicalMice KnockoutMice Inbred BALB CNFATC Transcription FactorsbiologyChemistryInterleukin-9T-Lymphocytes Helper-InducerUp-RegulationCell biologyMice Inbred C57BLAutocrine CommunicationCytokinemedicine.anatomical_structurebiology.proteinInterleukin-3030215 immunologyThe Journal of Immunology
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Mast cells control the expansion and differentiation of IL-10-competent B cells

2014

Abstract The discovery of B cell subsets with regulatory properties, dependent on IL-10 production, has expanded our view on the mechanisms that control inflammation. Regulatory B cells acquire the ability to produce IL-10 in a stepwise process: first, they become IL-10 competent, a poised state in which B cells are sensitive to trigger signals but do not actually express the Il-10 gene; then, when exposed to appropriate stimuli, they start producing IL-10. Even if the existence of IL-10–competent B cells is now well established, it is not yet known how different immune cell types cross talk with B cells and affect IL-10–competent B cell differentiation and expansion. Mast cells (MCs) contr…

Cell typeRegulatory B cellsCellular differentiationImmunologyCD40 LigandB-Lymphocyte SubsetsRegulatory B cellsB-cellBiologyExosomesLymphocyte ActivationImmunophenotypingMast cellMiceImmunophenotypingImmune systemmedicineImmunology and AllergyAnimalsMast CellsB cell differentiationCD40 AntigensB cellmast cell; IL-10; B-cellMice KnockoutCD40Cell DifferentiationCell biologyInterleukin-10Gastrointestinal TractInterleukin 10medicine.anatomical_structurePhenotypeMast cell; Regulatory B cells; IL-10; B cell differentiationImmunologyIL-10biology.proteinFemaleJournal of immunology (Baltimore, Md.
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Two mutations in gB-1 and gD-1 of herpes simplex virus type 1 are involved in the "fusion from without" phenotype in different cell types.

1996

Previous studies have shown that certain strains of herpes simplex viruses type 1 (HSV-1) are able to induce “fusion from without” (FFWO) which means no transcription or translation of the viral genome happens. The main determinants for FFWO in BHK cells are mutations in the C-terminal part of gB-1. But single mutations in this part of the genome are not sufficient to transfer the FFWO phenotype also to Vero cells. Here, we report that FFWO of HSV strains indeed need additional mutations in the N-terminal part of gD in order to produce the FFWO phenotype in BHK and Vero cells. By marker transfer we are able to show that loss of mutations in the N-terminal part of gD influences the ability t…

Cell typevirusesCellMolecular Sequence DataGenome ViralHerpesvirus 1 HumanBiologymedicine.disease_causeTransfectionGiant CellsVirusCell LineViral Envelope ProteinsTranscription (biology)VirologyCricetinaeChlorocebus aethiopsGeneticsmedicineBaby hamster kidney cellAnimalsHumansAmino Acid SequenceMolecular BiologyVero CellsBase SequenceGeneral MedicineVirologyPhenotypemedicine.anatomical_structureHerpes simplex virusPhenotypeDNA ViralMutationVero cellVirus genes
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Powerful tumor cell growth-inhibiting activity of a synthetic derivative of atractyligenin: Involvement of PI3K/Akt pathway and thioredoxin system

2014

The semi-synthetic ent-kaurane 15-ketoatractyligenin methyl ester (SC2017) has been previously reported to possess high antiproliferative activity against several solid tumor-derived cell lines. Our study was aimed at investigating SC2017 tumor growth-inhibiting activity and the underlying mechanisms in Jurkat cells (T-cell leukemia) and xenograft tumor models. METHODS: Cell viability was evaluated by MTT assay. Cell cycle progression, reactive oxygen species (ROS) elevation and apoptotic hallmarks were monitored by flow cytometry. Inhibition of thioredoxin reductase (TrxR) by biochemical assays. Levels and/or activation status of signaling proteins were assessed by western blotting. Xenogr…

CellBiophysicsAntineoplastic AgentsApoptosisAtractylosideBiologyCell cycleBiochemistryJurkat cellsMicePhosphatidylinositol 3-KinasesThioredoxinsTumor Cells CulturedmedicineAnimalsHumansMTT assayViability assaySettore BIO/15 - Biologia FarmaceuticaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationPI3K/AktHCT 116 xenograftCytochromes cApoptosiThioredoxin systemSettore CHIM/06 - Chimica OrganicaCell cycleXenograft Model Antitumor AssaysCell biologymedicine.anatomical_structureCaspasesCancer researchThioredoxinDiterpenes KauraneProto-Oncogene Proteins c-aktEnt-kaurane
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Invariant natural killer T cells act as an extravascular cytotoxic barrier for joint-invading Lyme Borrelia

2014

CXCR6-GFP(+) cells, which encompass 70% invariant natural killer T cells (iNKT cells), have been found primarily patrolling inside blood vessels in the liver. Although the iNKT cells fail to interact with live pathogens, they do respond to bacterial glycolipids presented by CD1d on liver macrophage that have caught the microbe. In contrast, in this study using dual laser multichannel spinning-disk intravital microscopy of joints, the CXCR6-GFP, which also made up 60-70% iNKT cells, were not found in the vasculature but rather closely apposed to and surrounding the outside of blood vessels, and to a lesser extent throughout the extravascular space. These iNKT cells also differed in behavior,…

CellMice TransgenicSpleenjoint iNKT cellsGranzymesMicegranzyme BmedicineAnimalsHumansCytotoxic T cellBorrelia burgdorferiImmunity CellularLyme DiseaseMice Inbred BALB CMultidisciplinarybiologyLyme arthritisNatural killer T cellbiology.organism_classificationGranzyme Bmedicine.anatomical_structureLiverGranzymeOrgan SpecificityBorrelia burgdorferiCD1DImmunologybiology.proteinNatural Killer T-CellsJointsJoint DiseasesSpleen
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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Immunotherapy With Human Gamma Delta T Cells—Synergistic Potential of Epigenetic Drugs?

2018

Epigenetics has emerged as one of the fastest growing concepts, adding more than 45 new publications every day, spreading through various fields ( 1). Conrad Waddington coined the term “epigenetics” in 1942; however, a multitude of definitions has been endorsed by different researchers. In essence, Waddington’s definition of “epigenetics” and its redefinition by Holiday is at the heart of cellular function. Hence, it is obvious that epigenetic regulation plays a central role also in the specification, differentiation, and functional plasticity of T lymphocytes ( 2). T-cell fate decision in progenitor cells, functional CD4 T-cell plasticity, CD8 T-cell differentiation, but also T-cell memory…

Checkpoint Inhibitorslcsh:Immunologic diseases. Allergy0301 basic medicineDeltaOpinionmedicine.medical_treatmentImmune checkpoint inhibitorsCell PlasticityImmunologyNatural-killer Group 2 Member DBiologyEpigenesis Genetic03 medical and health sciencesCell Plasticitymedicineddc:6AnimalsHumansgamma delta T cellsImmunology and Allergyddc:610EpigeneticsIntraepithelial Lymphocytesprogrammed death 1DNA methylationnatural-killer group 2 member DProgrammed Death 1articlehistone acetylationGamma Delta T CellsImmunotherapy030104 developmental biologyHistone acetylationDNA methylationCancer researchIntraepithelial lymphocyteBromodomain And Extraterminal DomainBromodomain and ExtraTerminal domainImmunotherapyimmunotherapyProgrammed death 1lcsh:RC581-607checkpoint inhibitorsFrontiers in Immunology
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Immunotoxicological in vitro effects of BEA and ENN B on Jurkat cell line

2016

ChemistryImmunologyGeneral MedicineLine (text file)ToxicologyMolecular biologyJurkat cellsIn vitroToxicology Letters
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Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia.

2003

Abstract Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophil…

ChemokineEpitopes T-LymphocyteImmunoglobulin Emedicine.disease_causeMiceCell MovementInfluenza A virusImmunology and AllergyEosinophiliaChemokine CCL5LungCells CulturedChemokine CCL2Mice KnockoutMice Inbred BALB Cbiologymedicine.diagnostic_testrespiratory systemUp-Regulationmedicine.anatomical_structureInfluenza A virusChemokines CCGoblet CellsNippostrongylusmedicine.symptomBronchial HyperreactivityChemokine CCL11OvalbuminImmunologyDown-RegulationMice TransgenicCCL5VirusInterferon-gammaTh2 CellsOrthomyxoviridae InfectionsLymphopeniamedicineAnimalsLymphocyte CountPulmonary EosinophiliaStrongylida InfectionsGoblet cellMetaplasiaAllergensPeptide Fragmentsrespiratory tract diseasesMice Inbred C57BLBronchoalveolar lavageImmunologyCell Migration Inhibitionbiology.proteinInterleukin-5Journal of immunology (Baltimore, Md. : 1950)
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