Search results for "interleukin-2"

showing 10 items of 269 documents

Lymphokine activated killer cells.

1989

Various subpopulations of human leukocytes may be induced by lymphokines to exert cytotoxic activity. In man major histocompatibility complex non-restricted tumor cell lysis by interleukin-2 (IL-2) induced peripheral blood lymphocytes is attributed mainly to natural killer cells. These T cell receptor negative large granular lymphocytes are called lymphokine activated killer (LAK) cells. In order to explore the potential of LAK cells in tumor therapy, several clinical studies have been conducted, using IL-2 alone or in combination with ex vivo IL-2-activated peripheral blood lymphocytes. Objective responses have reproducibly been achieved only in renal cell carcinoma and malignant melanoma …

Cytotoxicity ImmunologicLymphokine-activated killer cellTumor-infiltrating lymphocytesmedicine.medical_treatmentLymphokineHematologyGeneral MedicineImmunotherapyBiologyNatural killer T cellMajor histocompatibility complexLymphocyte ActivationTumor antigenKiller Cells NaturalImmunologymedicinebiology.proteinCytotoxic T cellAnimalsHumansInterleukin-2Killer Cells Lymphokine-ActivatedBlut
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T-T cell interactions during cytotoxic T cell responses. IV. Murine lymphoid dendritic cells are powerful stimulators for helper T lymphocytes.

1982

Enriched populations of Ia+ Fc receptor-negative dendritic cells were compared to other cell types for their stimulatory activity in primary mixed lymphocyte reactions to alloantigens and 2,4,6,-trinitrophenylated syngeneic cells. Dendritic cells were 20-100 times more effective than unfractionated splenocytes. A second cell type exhibiting strong stimulatory activity was an Ia+ Fc receptor-positive transiently adherent cell. Both types of stimulatory cells were only effective when able to produce the monokine interleukin 1. Thus glutaraldehyde-fixed cells were not stimulatory unless extraneous interleukin 1 was added. Stimulation of helper cells by either dendritic cells or Ia+ Fc receptor…

Cytotoxicity ImmunologicMaleRosette FormationMice Inbred AT cellT-LymphocytesImmunologyLymphocyte CooperationReceptors FcBiologyInterleukin 21MicemedicineImmunology and AllergyCytotoxic T cellAnimalsAntigens LyLymphocytesAntigen-presenting cellInterleukin 5Interleukin 3Mice Inbred BALB CLymphokine-activated killer cellImmune SeraHistocompatibility Antigens Class IICell biologyMice Inbred C57BLmedicine.anatomical_structureInterleukin 12Mice Inbred CBAInterleukin-2FemaleEuropean journal of immunology
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An Ovalbumin Peptide-Specific Cytotoxic T Cell Clone with Antigen Self-Presentation Capacity Uses Two Distinct Mechanisms to Kill Target Cells

1993

Abstract Cloned 10BK.1 T cells with specificity for the ovalbumin peptide OVA257-264 are representative of a novel cell type within the CD8 + subset of T cells. In the presence and in the absence of added antigen presenting cells these T cells react toward antigen (Ag) by proliferation and lymphokine production. These data suggest self-presentation of the Ag by 10BK.1 cells. Here we present evidence that 10BK.1 cells exhibit cytotoxic activity that involves two different cytotoxic effector mechanisms. (i) One mechanism is fast killing activity, apparent within 4 hr. Constitutive mouse T cell-specific proteinase-1 (MTSP-1) activity, constitutive expression of MTSP-1 RNA, increased by Ag chal…

Cytotoxicity ImmunologicPore Forming Cytotoxic ProteinsOvalbuminImmunologyAntigen presentationAntigen-Presenting CellsBiologyCytoplasmic GranulesLymphocyte ActivationGranzymesCell LineMiceInterleukin 21AntigenAnimalsCytotoxic T cellIL-2 receptorAntigen-presenting cellLymphotoxin-alphaMembrane GlycoproteinsCD40PerforinTumor Necrosis Factor-alphaSerine EndopeptidasesDegranulationMolecular biologyClone Cellsbiology.proteinInterleukin-2T-Lymphocytes CytotoxicCellular Immunology
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Frequency of cytotoxic T lymphocyte precursors to herpes simplex virus type 1 as determined by limiting dilution analysis.

1983

The conditions for establishing a limiting dilution assay to measure cytotoxic T lymphocyte precursors (CTL-P) against herpes simplex virus type 1 (HSV-1) were determined. Analysis by Poisson statistics demonstrated that the estimated frequency of HSV-1-reactive cells in the spleens of normal mice was less than 1/250,000. In contrast, mice immunized previously with infectious HSV-1 demonstrated a CTL-P frequency between 1/3,500 and 1/15,670. The generation of a maximum cytotoxic T lymphocyte response required that mice be primed in vivo with infectious virus. Immunization with inactivated virus either failed to elicit detectable CTL-P frequencies or gave frequencies markedly less than thos…

Cytotoxicity ImmunologicT cellImmunologyPopulationchemical and pharmacologic phenomenaBiologymedicine.disease_causeMicrobiologyVirusMiceImmune systemAntigenmedicineCytotoxic T cellAnimalsAntigens LySimplexviruseducationCytotoxicityCells Culturededucation.field_of_studyVirologyInfectious Diseasesmedicine.anatomical_structureHerpes simplex virusImmunologic TechniquesMice Inbred CBAInterleukin-2ParasitologyImmunizationSpleenT-Lymphocytes CytotoxicViral Infections and ImmunityInfection and immunity
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Cyclosporin A mediates immunosuppression of primary cytotoxic T cell responses by impairing the release of interleukin 1 and interleukin 2

1981

The site of action of the immunosuppressive drug cyclosporin A in in vitro cytotoxic allograft responses has been localized. General cytotoxic effects of the drug on proliferating T cells became apparent at concentrations of 500-1000 ng/ml, while selective effects were observed at concentrations of 10-100 ng/ml. The selective effects included a blockade of interleukin 2 release from activated T helper cells on the one hand and inhibition of interleukin 1 release from splenic adherent cells on the other. While cyclosporin A did not interfere with the intracellular events required for the activation and subsequent clonal expansion of alloreactive T cells, the lack of interleukin 1 and interle…

Cytotoxicity ImmunologicT-LymphocytesImmunologyCyclosporinsPharmacologyBiologyLymphocyte ActivationMiceInterleukin 21Cyclosporin aAnimalsImmunology and AllergyInterleukin 5Interleukin 4Interleukin 3Mice Inbred BALB CProteinsInterleukinInterleukin 33Protein BiosynthesisMice Inbred CBAInterleukin 12Interleukin-2Lymphocyte Culture Test MixedImmunosuppressive AgentsInterleukin-1European Journal of Immunology
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Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis.

2005

Abstract In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, immunization with myelin Ags leads to demyelination and paralysis. To investigate which molecules are crucial for the pathogenesis of EAE, we specifically assessed the roles of the death receptors Fas and TNF-R1. Mice lacking Fas expression in oligodendrocytes (ODCs) were generated and crossed to TNF-R1-deficient mice. To achieve specific deletion of a loxP-flanked fas allele in ODCs, we generated a new insertion transgene, expressing the Cre recombinase specifically in ODCs. Fas inactivation alone as well as the complete absence of TNF-R1 protected mice partially from EAE induced by the imm…

Encephalomyelitis Autoimmune ExperimentalEncephalomyelitisTransgeneT-LymphocytesImmunologyApoptosisMyelin oligodendrocyte glycoproteinMyelinInterferon-gammaMicemedicineImmunology and AllergyAnimalsfas ReceptorReceptorInflammationbiologyMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.diseaseMice Inbred C57BLMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologybiology.proteinInterleukin-2Myelin-Oligodendrocyte GlycoproteinMyelin ProteinsDemyelinating DiseasesJournal of immunology (Baltimore, Md. : 1950)
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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Differential effects of anti-TNF-α and anti-IL-12/23 agents on human leukocyte–endothelial cell interactions

2015

AbstractEnhanced leukocyte recruitment is an inflammatory process that occurs during early phases of the vascular dysfunction that characterises atherosclerosis. We evaluated the impact of anti-TNF-α (adalimumab, infliximab and etanercept) and anti-IL-12/23 (ustekinumab) on interactions between human leukocytes and endothelial cells in a flow chamber that reproduced in vivo conditions. Clinical concentrations of anti-TNF-α were evaluated on the leukocyte recruitment induced by a variety of endothelial (TNF-α, interleukin-1β, lymphotoxin-α and angiotensin-II) and leukocyte (PAF, IL-12 and IL-23) stimuli related to inflammation and atherosclerosis. Treatment with anti-TNF-α, even before or af…

EndotheliumInflammationAnti-IL-12/23 agentsCardiovascular side effectsBiologicsInterleukin-23Rheumatic diseasesIn vivoPsoriasisHuman Umbilical Vein Endothelial CellsInterleukin 23HumansMedicineAnti-TNF-α agentsPharmacologyTumor Necrosis Factor-alphabusiness.industryCell adhesion moleculeAdalimumabEndothelial Cellsmedicine.diseaseInterleukin-12Leukocyte–endothelial cell interactionsEndothelial stem cellmedicine.anatomical_structureImmunologyLeukocytes MononuclearTumor necrosis factor alphamedicine.symptombusinessEuropean Journal of Pharmacology
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Sumoylation of the transcription factor NFATc1 leads to its subnuclear relocalization and interleukin-2 repression by histone deacetylase.

2009

The family of NFAT (nuclear factor of activated T-cells) transcription factors plays an important role in cytokine gene regulation. In peripheral T-cells NFATc1 and -c2 are predominantly expressed. Because of different promoter and poly(A) site usage as well as alternative splicing events, NFATc1 is synthesized in multiple isoforms. The highly inducible NFATc1/A contains a relatively short C terminus, whereas the longer, constitutively expressed isoform NFATc1/C spans an extra C-terminal peptide of 246 amino acids. Interestingly, this NFATc1/C-specific terminus can be highly sumoylated. Upon sumoylation, NFATc1/C, but not the unsumoylated NFATc1/A, translocates to promyelocytic leukemia nuc…

Gene isoformSUMO proteinBiologyBiochemistryHistone DeacetylasesCell LineMiceAnimalsHumansProtein IsoformsMolecular BiologyTranscription factorRegulation of gene expressionCell NucleusLymphokinesintegumentary systemNFATC Transcription FactorsActivator (genetics)Mechanisms of Signal TransductionNFATCell BiologyMolecular biologyChromatinHistoneGene Expression RegulationUbiquitin-Conjugating Enzymesbiology.proteinSmall Ubiquitin-Related Modifier ProteinsInterleukin-2Histone deacetylaseThe Journal of biological chemistry
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Cutting Edge: TGF-β Signaling Is Required for the In Vivo Expansion and Immunosuppressive Capacity of Regulatory CD4+CD25+ T Cells

2004

Abstract Data regarding the role of TGF-β for the in vivo function of regulatory CD4+CD25+ T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-β signaling specifically in T cells was used to assess the role of endogenous TGF-β for the in vivo function of CD4+CD25+ Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4+CD25+ Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4+CD25+ Treg we could demonstrate that endogenous TGF-β promotes the expansion of CD4+CD25+ Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4+CD25+ Treg and were …

Genetically modified mouseAdoptive cell transferTransgeneImmunologychemical and pharmacologic phenomenaEndogenyBiologyT-Lymphocytes RegulatoryMiceTransforming Growth Factor betaIn vivomedicineAnimalsHumansImmunology and AllergyGenetic Predisposition to DiseaseLymphocyte CountIL-2 receptorColitisReceptorCell DifferentiationReceptors Interleukin-2hemic and immune systemsColitismedicine.diseaseAdoptive TransferCell biologyImmunologySignal TransductionThe Journal of Immunology
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