Search results for "Differentiation"

showing 10 items of 1605 documents

Granulysin‐Dependent Killing of Intracellular and ExtracellularMycobacterium tuberculosisby Vγ9/Vδ2 T Lymphocytes

2001

Contribution of Vgamma9/Vdelta2 T lymphocytes to immune protection against Mycobacterium tuberculosis is still a matter of debate. It was reported earlier that Vgamma9/Vdelta2 T lymphocytes kill macrophages harboring live M. tuberculosis through a granule-dependent mechanism that results in killing of intracellular bacilli. This study found that Vgamma9/Vdelta2 T lymphocytes reduce the viability of both extracellular and intracellular M. tuberculosis. Granulysin and perforin, both detected in Vgamma9/Vdelta2 T lymphocytes, play a major role, which indicates that Vgamma9/Vdelta2 T lymphocytes directly contribute to a protective host response against M. tuberculosis infection.

Antigens Differentiation T-LymphocyteCytotoxicity ImmunologicTuberculosisReceptors Antigen T-Cell alpha-betaT-LymphocytesBiologyMicrobiologyMycobacterium tuberculosisExtracellularmedicineHumansTuberculosisImmunology and AllergyMacrophageGranulysinMacrophagesReceptors Antigen T-Cell gamma-deltaMycobacterium tuberculosisT lymphocytemedicine.diseasebiology.organism_classificationInfectious DiseasesPerforinImmunologybiology.proteinIntracellularThe Journal of Infectious Diseases
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Enzymatic Activity of CD26 (Dipeptidylpeptidase IV) is not Required for Its Signalling Function in T Cells

1993

Abstract CD26 is a proteolytic enzyme (dipeptidylpeptidase IV) expressed on the T cell surface that defines an alternative activation signal for human T lymphocytes. Crosslinking of CD26 via monoclonal antibodies triggers proliferation and cytotoxicity in preactivated T cells. In this study, we used highly specific competitive and irreversible inhibitors of dipeptidylpeptidase IV to study the role of the enzymatic activity in activation of CD26- transfected T cells as well as of CD26-expressing normal human T cell clones. These inhibitors at concentrations that blocked up to 95% of the enzymatic activity, did not specifically inhibit T cell activation neither via TCR/CD3 nor via CD26 itself…

Antigens Differentiation T-LymphocyteDipeptidyl Peptidase 4T-LymphocytesT cellCD3ImmunologyBiologyLymphocyte ActivationCell LineMiceTumor Cells CulturedmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellDipeptidyl-Peptidases and Tripeptidyl-PeptidasesT-cell receptorProteolytic enzymesHematologyTransfectionT lymphocyteCytotoxicity Tests ImmunologicCell biologymedicine.anatomical_structureBiochemistrybiology.proteinInterleukin-2Clone (B-cell biology)Signal TransductionImmunobiology
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Function of Dipeptidyl Peptidase IV (CD26, Tp103) in Transfected Human T Cells

1993

CD26 (Tp103) is a proteolytic enzyme (dipeptidyl peptidase IV) expressed on the T cell surface that defines an alternative activation signal for human T lymphocytes. It is absent from or present in only low amounts on resting T cells but it is expressed strongly after activation. Crosslinking of CD26/Tp103 via the monoclonal antibody CB.1 triggers functional activities in preactivated T cells. To study the molecular requirements for T cell activation via CD26 we transfected a cDNA encoding CD26 into several CD26-negative cells. In Jurkat T cell leukemia cells that normally do not express the CD26 antigen, the transfected CD26 molecule is functional because the monoclonal antibody CB.1 induc…

Antigens Differentiation T-LymphocyteDipeptidyl Peptidase 4T-LymphocytesT cellZAP70ImmunologyT-cell receptorReceptors Antigen T-CellBiologyTransfectionNatural killer T cellMolecular biologyJurkat cellsRecombinant ProteinsCell LineMicemedicine.anatomical_structureAntigenTumor Cells CulturedmedicineAnimalsHumansCytotoxic T cellIL-2 receptorDipeptidyl-Peptidases and Tripeptidyl-PeptidasesCellular Immunology
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T cells can present antigens such as HIV gp120 targeted to their own surface molecules

1988

To trigger class II-restricted T cells, antigen presenting cells have to capture antigens, process them and display their fragments in association with class II molecules. In most species, activated T cells express class II molecules; however, no evidence has been found that these cells can present soluble antigens. This failure may be due to the inefficient capture, processing or display of antigens in a stimulatory form by T-cells. The capture of a soluble antigen, which is achieved by nonspecific mechanisms in macrophages and dendritic cells, can be up to 10(3) times more efficient in the presence of surface receptors, such as surface immunoglobulin on B cells that specifically bind anti…

Antigens Differentiation T-LymphocyteHerpesvirus 4 HumanImmunoprecipitationSurface ImmunoglobulinT-LymphocytesAntigen presentationRetroviridae ProteinsAntigen-Presenting CellsHIV Envelope Protein gp120Viral Envelope ProteinsAntigenHistocompatibility AntigensHumansAntigen-presenting cellAntigens ViralCell Line TransformedB-LymphocytesMultidisciplinarybiologyAntibodies MonoclonalHIVMolecular biologyCell culturebiology.proteinAntibodyCD8Nature
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Involvement of soluble mediator(s) different from interleukin (IL)1 in the antigen-induced IL 2 receptor expression and proliferation of L3T4+ (CD4+)…

1988

Proliferation of T lymphocytes (T cells) requires the interaction of interleukin 2 (IL 2) with the high affinity form of the IL 2 receptor (IL 2R). IL 2 production as well as IL 2R expression are generally induced simultaneously in T cells by the recognition of specific antigen displayed on the surface of syngeneic antigen-presenting cells. The experiments described herein show that the expression of IL 2R has different requirements than the production of IL 2 (and other lymphokines). Stimulation of antigen-specific L3T4+ T cell lines with antigen-pulsed spleen cells (SC) treated with ultraviolet (UV) light results in efficient IL 2 production but only minimal proliferation due to reduced I…

Antigens Differentiation T-LymphocyteInterleukin 2Ultraviolet RaysT-LymphocytesT cellImmunologyAntigen-Presenting CellsBiologyLymphocyte ActivationMiceInterleukin 21medicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigensReceptors ImmunologicInterleukin 3Mice Inbred BALB CMice Inbred C3HLymphokineReceptors Interleukin-2Molecular biologymedicine.anatomical_structureGene Expression RegulationImmunologyInterleukin 12Interleukin-2Cell DivisionSpleenmedicine.drugEuropean Journal of Immunology
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Peritoneal Cavity is a Route for Gut-Derived Microbial Signals to Promote Autoimmunity in Non-Obese Diabetic Mice

2015

Macrophages play a crucial role in innate immune reactions, and peritoneal macrophages (PMs) guard the sterility of this compartment mainly against microbial threat from the gut. Type 1 diabetes (T1D) is an autoimmune disease in which gut microbiota and gut immune system appear to contribute to disease pathogenesis. We have recently reported elevated free radical production and increased permeability of gut epithelium in non-obese diabetic (NOD) mice. Impaired barrier function could lead to bacterial leakage to the peritoneal cavity. To explore the consequences of impaired gut barrier function on extra-intestinal immune regulation, we characterized peritoneal lavage cells from young newly w…

Antigens Differentiation T-LymphocyteLipopolysaccharidesmedicine.medical_specialtymiceT-LymphocytesT cellBlotting WesternImmunologyWeaningNodBiologyta3111Peritoneal cavityImmune systemSpecies SpecificityAntigens CDMice Inbred NODInternal medicinediabeticmedicineAnimalsLectins C-TypeIntestinal Mucosamicrobial signalsCells CulturedNOD miceMice Inbred BALB CInnate immune systemTumor Necrosis Factor-alphanon-obeseMicrobiotaautoimmunityta1182ta3141General MedicineFlow CytometryGut EpitheliumIntestinesMice Inbred C57BLInterleukin-1 Receptor-Associated KinasesEndocrinologymedicine.anatomical_structureperitoneal cavityImmunologyMacrophages PeritonealTumor necrosis factor alphaInjections IntraperitonealSignal TransductionScandinavian Journal of Immunology
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Mycobacterial antigen(s) induce anergy by altering TCR- and TCR/CD28-induced signalling events: insights into T-cell unresponsiveness in leprosy.

2009

Present study investigates the role of Mycobacterium leprae (M. leprae) antigens on TCR- and TCR/CD28-induced signalling leading to T-cell activation and further correlates these early biochemical events with T-cell anergy, as prevailed in advanced stages of leprosy. We observed that both whole cell lystae (WCL) and soluble fraction of M. leprae sonicate (MLSA) not only inhibited TCR, thapsigargin and ionomycin induced calcium fluxes by diminishing the opening of calcium channels, but also TCR- or TCR/CD28-induced proximal signalling events like phosphorylation of Zap-70 and protein kinase-C (PKC) activity. Study of TCR- and TCR/CD28-induced downstream signals revealed that M. leprae antige…

Antigens Differentiation T-LymphocyteMAP Kinase Signaling SystemT cellT-LymphocytesImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyLymphocyte ActivationJurkat cellsp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundJurkat CellsCD28 AntigensAntigens CDLeprosyCalcium fluxmedicineHumansLectins C-TypeEnzyme InhibitorsPromoter Regions GeneticMolecular BiologyMycobacterium lepraeProtein Kinase CCell ProliferationClonal AnergyAntigens BacterialMitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinaseIonophoresNFATC Transcription FactorsIonomycinT-cell receptorInterleukin-2 Receptor alpha SubunitCD28hemic and immune systemsNFATbiology.organism_classificationCell biologyMycobacterium lepraemedicine.anatomical_structurechemistryGene Expression RegulationIonomycinImmunologyInterleukin-2ThapsigarginCalciumMolecular immunology
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Overexpression of genes involved in lymphocyte activation and regulation are associated with reduced CRM-derived cardiac remodelling after STEMI

2021

Abstract Aims Lymphopenia after ST-segment elevation myocardial infarction (STEMI) correlates with deleterious cardiac consequences and worse prognosis. An in-depth examination of genes implicated in lymphocyte proliferation, activation and regulation and their association with short- and long-term cardiac structure and function is therefore of great interest. Methods Peripheral blood mononuclear cells were isolated from 10 control subjects and 64 patients with a first STEMI treated with primary percutaneous coronary intervention and submitted to cardiac magnetic resonance after 1 week and 6 months. mRNA expression of genes implicated in lymphocyte activation (CD25 and CD69) and regulation …

Antigens Differentiation T-LymphocyteMale0301 basic medicinemedicine.medical_specialtyLymphocytemedicine.medical_treatmentProgrammed Cell Death 1 ReceptorImmunologyGene Expressionchemical and pharmacologic phenomenaLymphocyte proliferationLymphocyte Activation03 medical and health sciences0302 clinical medicineAntigens CDInternal medicineHumansImmunology and AllergyMedicineCytotoxic T cellCTLA-4 AntigenLectins C-TypeIL-2 receptorMyocardial infarctionGeneAgedPharmacologyVentricular Remodelingbusiness.industryInterleukin-2 Receptor alpha SubunitPercutaneous coronary interventionHearthemic and immune systemsOdds ratioMiddle Agedmedicine.diseaseMagnetic Resonance ImagingPathophysiology030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchLymphocyte activationLeukocytes MononuclearCardiologyST Elevation Myocardial InfarctionFemaleCardiology and Cardiovascular MedicinebusinessInternational Immunopharmacology
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Missense mutations in the fas gene resulting in autoimmune lymphoproliferative syndrome: A molecular and immunological analysis

1997

AbstractProgrammed cell death (or apoptosis) is a physiological process essential to the normal development and homeostatic maintenance of the immune system. The Fas/Apo-1 receptor plays a crucial role in the regulation of apoptosis, as demonstrated by lymphoproliferation in MRL-lpr/lpr mice and by the recently described autoimmune lymphoproliferative syndrome (ALPS) in humans, both of which are due to mutations in the Fas gene. We describe a novel family with ALPS in which three affected siblings carry two distinct missense mutations on both the Fas gene alleles and show lack of Fas-induced apoptosis. The children share common clinical features including splenomegaly and lymphadenopathy, b…

Antigens Differentiation T-LymphocyteMaleAdolescentT-LymphocytesCD3ImmunologyLymphoproliferative disordersBiologyLymphocyte ActivationAutoimmune DiseaseBiochemistryFas ligandImmunophenotypingImmune systemPedigree; Antigens Differentiation T-Lymphocyte; Solubility; Apoptosis; Autoimmune Diseases; Humans; Antigens CD95; Child; Lymphocytes; Child Preschool; Lymphocyte Activation; Syndrome; Lymphoproliferative Disorders; Adolescent; Mutation; Immunophenotyping; Male; Biological Markers; T-LymphocytesmedicineChildAutoimmune diseaseApoptosiSyndromeCell BiologyHematologymedicine.diseaseFas receptorPedigreeAntigens CD95SolubilityApoptosisChild PreschoolLymphoproliferative DisorderAutoimmune lymphoproliferative syndromeMutationBiological MarkerImmunologybiology.proteinLymphocyteHuman
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Selective depression of interferon-γ and granulysin production with increase of proliferative response by Vγ9/Vδ2 T cells in children with tuberculos…

2002

Vgamma9/Vdelta2 T cells can contribute to protective immune response against Mycobacterium tuberculosis, although the extent to which and mechanisms by which they could actually protect against human tuberculosis remain unclear. We have previously reported that Vgamma9/Vdelta2 T cells from tuberculin purified protein derivative (PPD)-positive children, either healthy or affected by different clinical forms of tuberculosis, strongly proliferate to different phosphoantigens in vitro, whereas Vgamma9/Vdelta2 T cells from PPD-negative healthy subjects proliferate very poorly. We report here that Vgamma9/Vdelta2 T cells from tuberculous children have an increased proliferative activity, but decr…

Antigens Differentiation T-LymphocyteMaleAdolescentTuberculosiT cellT-LymphocytesAntitubercular AgentsMycobacterium tuberculosis.BiologyMycobacterium tuberculosisAntitubercular AgentInterferon-gammaImmune systemAntigenmedicineImmunology and AllergyCytotoxic T cellHumansTuberculosisInterferon gammaGranulysinChildTuberculin TestInfantReceptors Antigen T-Cell gamma-deltaMycobacterium tuberculosisbiology.organism_classificationInfectious Diseasesmedicine.anatomical_structureGranulysin productionT-LymphocyteChild PreschoolImmunologyFemalemedicine.drugHuman
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