Search results for "Immune System"

showing 10 items of 2885 documents

Depletion of alloreactive T cells via CD69: implications on antiviral, antileukemic and immunoregulatory T lymphocytes

2005

Selective depletion of alloreactive T cells from stem-cell allografts should abrogate graft-versus-host disease while preserving beneficial T cell specificities to facilitate engraftment and immune reconstitution. We therefore explored a refined immunomagnetic separation strategy to effectively deplete alloreactive donor lymphocytes expressing the activation antigen CD69 upon stimulation, and examined the retainment of antiviral, antileukemic, and immunoregulatory T cells. In addition to the CD69high T cell fraction, our studies retrieved two T cell subsets based on residual CD69 expression. Whereas, truly CD69(neg) cells were devoid of detectable alloresponses to original stimulators, CD69…

Antigens Differentiation T-LymphocyteCD4-Positive T-LymphocytesEpstein-Barr Virus InfectionsHerpesvirus 4 HumanT cellCytomegalovirusGraft vs Host DiseaseCell Cycle Proteinschemical and pharmacologic phenomenaStreptamerBiologyLymphocyte ActivationLymphocyte DepletionCell LineInterleukin 21Antigens CDmedicineHumansTransplantation HomologousCytotoxic T cellLectins C-TypeIL-2 receptorAntigen-presenting cellTransplantationHematopoietic Stem Cell TransplantationNuclear ProteinsForkhead Transcription FactorsReceptors Interleukin-2hemic and immune systemsHematologyT lymphocyteNatural killer T cellDNA-Binding Proteinsmedicine.anatomical_structureCytomegalovirus InfectionsImmunologyRNA Splicing FactorsCarrier ProteinsImmunologic MemoryBone Marrow Transplantation
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Identification of epitopes of Mycobacterium tuberculosis 16-kDa protein recognized by human leukocyte antigen-A*0201 CD8(+) T lymphocytes.

2002

CD8(+) T cells could make an important contribution to protection against tuberculosis (TB), but the antigenic determinants recognized in the context of major histocompatibility complex class I molecules remain ill defined. Our aim was to identify nonamer peptides derived from the acr/16-kDa antigen. Two immunogenic peptides (p21-29 and p120-128) were identified by their ability to elicit cytotoxic CD8(+) T cells from juvenile patients recovering from TB. Epitope-specific recognition was demonstrated by the lysis of both Mycobacterium tuberculosis-infected and peptide-pulsed macrophages, the release of cytotoxic granules, and interferon-gamma and tumor necrosis factor-alpha production. CD8(…

Antigens Differentiation T-LymphocyteCytotoxicity ImmunologicMalePore Forming Cytotoxic ProteinsT cellEpitopes T-LymphocyteHuman leukocyte antigenCD8-Positive T-LymphocytesMajor histocompatibility complexEpitopeInterferon-gammaImmune systemAntigenBacterial ProteinsHLA-A2 AntigenmedicineImmunology and AllergyCytotoxic T cellHumansChildTuberculosis PulmonaryMembrane GlycoproteinsbiologyHLA-A AntigensPerforinTumor Necrosis Factor-alphaMacrophagesMycobacterium tuberculosisFlow CytometryPeptide FragmentsMolecular WeightInfectious Diseasesmedicine.anatomical_structureImmunologybiology.proteinFemaleCD8The Journal of infectious diseases
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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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Inducible Co-Stimulator Null MRL-Fas lpr Mice

2005

MRL/MpJ-Tnfrsf6lpr (MRL-Faslpr) mice develop a spontaneous T cell-dependent autoimmune disease that shares features with human lupus, including fatal nephritis, systemic pathology, and autoantibodies (autoAb). The inducible co-stimulator (ICOS) is upregulated on activated T cells and modulates T cell-mediated responses. To investigate whether ICOS has an essential role in regulating autoimmune lupus nephritis and the systemic illness in MRL-Faslpr mice, ICOS null (-/-) MRL Faslpr and ICOS intact (+/+) MRL-Faslpr strains (wild-type [WT]) were generated and compared. It was determined that in ICOS-/- MRL-Faslpr as compared with the WT strain, (1) there is a significant reduction in circulatin…

Antigens Differentiation T-LymphocyteMice Inbred MRL lprT-LymphocytesT cellLupus nephritismedicine.disease_causeBlood Urea NitrogenAutoimmunityInducible T-Cell Co-Stimulator ProteinInterferon-gammaMiceImmune systemimmune system diseasesmedicineAnimalsskin and connective tissue diseasesAutoantibodiesMice Inbred C3HSystemic lupus erythematosusTumor Necrosis Factor-alphabusiness.industryAutoantibodyGeneral Medicinemedicine.diseaseLupus NephritisIsotypeInterleukin-10Mice Inbred C57BLProteinuriamedicine.anatomical_structureNephrologyImmunoglobulin GImmunologyInterleukin-4businessNephritisJournal of the American Society of Nephrology
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Stimulator cell-dependent requirement for CD2- and LFA-1-mediated adhesions in T lymphocyte activation by superantigenic toxins.

1992

Abstract The staphylococcal enterotoxins and related microbial T cell mitogens stimulate T cells by cross-linking variable parts of the T cell receptor (TCR) with MHC class II molecules on accessory or target cells. We have used cloned human T cells and defined tumor cells as accessory cells (AC) to study the requirements for T cell activation by these toxins. On AC expressing high levels of CD54 (intercellular adhesion molecule-1, ICAM-1) and CD58 (lymphocyte function-associated antigen-3, LFA-3), mAb to CD2 were relatively ineffective in inhibiting the response to the toxins and antibodies to the lymphocyte function-associated antigen-1 (LFA-1) did not inhibit at all. If added together, h…

Antigens Differentiation T-LymphocyteT cellImmunologyBacterial ToxinsCD2 AntigensAntigen-Presenting Cellschemical and pharmacologic phenomenaStreptamerBiologyIn Vitro TechniquesLymphocyte ActivationT-Lymphocyte SubsetsmedicineCell AdhesionCytotoxic T cellHumansIL-2 receptorReceptors ImmunologicAntigen-presenting cellAntigens ViralCells CulturedAntigens BacterialMembrane GlycoproteinsCD28hemic and immune systemsT lymphocyteNatural killer T cellCD58 AntigensIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Cell biologymedicine.anatomical_structureImmunologyAntigens SurfaceCell Adhesion MoleculesCellular immunology
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T cell activation defect in hemodialysis patients: Evidence for a role of the B7/CD28 pathway

1993

T cell activation defect in hemodialysis patients: Evidence for a role of the B7/CD28 pathway. The immunosuppressive effect of chronic renal failure is correlated with an impaired proliferation of peripheral blood leukocytes in vitro . This is mainly due to an impaired function of the accessory cells rather than the T cells. Here we tried to define a missing accessory signal for T cell activation in hemodialysis patients. We substituted cell surface bound molecules by adding tumor cell lines to the in vitro assays that express different patterns of accessory molecules. Cell lines that express the costimulatory B7 molecule reconstituted the activation of patients' cells whereas B7 negative c…

Antigens Differentiation T-LymphocyteT-LymphocytesT cellCellLymphocyte ActivationTransfectionMonocytesMiceImmune systemCD28 AntigensAntigens CDRenal DialysisTumor Cells CulturedmedicineAnimalsHumansPhytohemagglutininsAntigen-presenting cellAgedUremiabusiness.industryCD283T3 CellsT lymphocyteTransfectionMiddle AgedBurkitt LymphomaPhenotypemedicine.anatomical_structureNephrologyCell cultureAntigens SurfaceImmunologyB7-1 AntigenCancer researchInterleukin-2businessKidney International
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