Search results for " ACTIVATION"

showing 10 items of 1535 documents

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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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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Alternative pathway activation of T cells by binding of CD2 to its cell-surface ligand.

1987

Activation of resting T lymphocytes is initiated by the interaction of cell-surface receptors with their corresponding ligands. In addition to activation through the CD3 (T3)-Ti antigen-receptor complex1, recent experiments have demonstrated induction of T-cell proliferation through the CD2 (T11) molecule2–4, traditionally known as the erythrocyte(E)-receptor, through which T cells can bind red blood cells (RBC)5–7. This 'alternative pathway' of T-cell activation2 was observed in vitro in response to combinations of anti-CD2 monoclonal antibodies (mAbs) that bind to distinct epitopes of CD2, such as mAbs against T112 plus T113 (ref. 2). The physiological importance of this activation pathwa…

Antigens Differentiation T-LymphocyteMultidisciplinaryErythrocytesRosette FormationbiologyCD3T-LymphocytesDose-Response Relationship ImmunologicAntibodies MonoclonalLigandsLymphocyte ActivationMolecular biologyIn vitroCD2 moleculeEpitopeCell biologyCell surface receptorAntigens SurfaceAlternative complement pathwaybiology.proteinHumansIL-2 receptorReceptorNature
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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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An antigen-independent physiological activation pathway for L3T4+ T lymphocytes.

1987

The data presented in this report describe an antigen-independent activation pathway leading to reinduction of proliferation of class II major histocompatibility complex (MHC)-restricted murine T cell lines that after previous antigen-specific stimulation reverted to a resting state. Antigen-independent proliferation and interleukin 2 (IL2)-receptor expression occur in the presence of splenic accessory cells, exogenous IL2 and a soluble factor(s) provisionally termed T cell-stimulating factor(s) (TSF). Each of these components is essential for inducing growth. TSF is found in the supernatant of an autoreactive T cell line upon stimulation with syngeneic accessory cells. Neither TSF nor acce…

Antigens Differentiation T-LymphocyteT cellImmunologyReceptors Antigen T-CellMice Inbred StrainsGrowthBiologyMajor histocompatibility complexLymphocyte ActivationCell LineTosyl CompoundsMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorAntigensReceptors ImmunologicAntigen-presenting cellMice Inbred BALB CHistocompatibility Antigens Class IICD28Receptors Interleukin-2T-Lymphocytes Helper-InducerCell biologymedicine.anatomical_structurePhenotypeImmunologyAntigens Surfacebiology.proteinInterleukin-2CD8SpleenEuropean journal of immunology
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The role of ICOS in directing T cell responses: ICOS-dependent induction of T cell anergy by tolerogenic dendritic cells.

2009

Abstract Tolerogenic dendritic cells (DC) play an important role in maintaining peripheral T cell tolerance in steady-state conditions through induction of anergic, IL-10-producing T cells with suppressive properties. ICOS, an activation-induced member of the CD28 family on T cells, is involved in the induction of IL-10, which itself could contribute to induction of anergy and development of suppressive T cells. Therefore, we analyzed the functional role of ICOS in the differentiation process of human CD4+ T cells upon their interaction with tolerogenic DC. We compared the functional properties of CD4+ T cells from healthy volunteers and ICOS-deficient patients after stimulation with tolero…

Antigens Differentiation T-LymphocyteT cellT-LymphocytesImmunologyLymphocyte ActivationT-Lymphocytes RegulatoryInducible T-Cell Co-Stimulator ProteinInterleukin 21medicineImmunology and AllergyCytotoxic T cellHumansIL-2 receptorAntigen-presenting cellCells CulturedClonal AnergyChemistryPeripheral toleranceCell DifferentiationDendritic CellsNatural killer T cellCoculture TechniquesCell biologyInterleukin-10ICOS LIGANDmedicine.anatomical_structureCommon Variable ImmunodeficiencyGene Knockdown TechniquesImmunologyJournal of immunology (Baltimore, Md. : 1950)
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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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CD2-mediated autocrine growth of herpes virus saimiri-transformed human T lymphocytes.

1992

Herpes virus saimiri (HVS) immortalizes T lymphocytes from a variety of primates and causes acute T cell lymphomas and leukemias in nonnatural primate hosts. Here we have analyzed the requirements for growth of three HVS-transformed human T cell lines. The cells expressed the phenotype of activated T cells: two were CD4+, and one was CD8+. All three cells responded to all allogeneic human cell lines tested with enhanced proliferation, production of interleukin 2 (IL-2), and increased expression of the IL-2 receptor. Binding of CD2 to its ligand CD58 was the critical event mediating stimulation because: (a) monoclonal antibodies (mAbs) to CD2 and to CD58, but not to a variety of other surfac…

Antigens Differentiation T-LymphocyteT-LymphocytesT cellImmunologyCD2 AntigensBiologyLymphocyte ActivationHerpesvirus 2 SaimiriineInterleukin 21medicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorReceptors ImmunologicAntigen-presenting cellInterleukin 3ArticlesCell Transformation ViralNatural killer T cellVirologyMolecular biologyPhenotypemedicine.anatomical_structureInterleukin 12Interleukin-2Cell DivisionJournal of Experimental Medicine
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