Search results for "Lymphotoxin-alpha"

showing 7 items of 7 documents

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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Cytokine production pathway in the elderly.

1996

It is well known that aging is associated with various alterations in lymphoid cell functions, particularly with a progressive decline in immune responsiveness to exogenous antigens and increasing incidence of autoimmune phenomena. Many studies have been focused on the mechanisms of the immunologic features of aging. this review describes our results of studies performed to determine the influence of age on the capacity to produce interleukin-2 (IL-2), interferon-gamma (IFN-gamma), interleukin-4 (IL-4), interleukin-t (IL-5), interleukin-6 (IL-6) and tumor necrosis factor (TNF). Mitogen-stimulated cultures of mononuclear cells (MNC) from human beings were assessed for cytokine-producing capa…

Interleukin 2Agingmedicine.medical_treatmentT cellT-LymphocytesImmunologyBiologyIn Vitro TechniquesLymphocyte ActivationInterferon-gammaMiceImmune systemAntigenmedicineAnimalsHumansInterferon gammaLymphotoxin-alphaImmunodeficiencyAgedmedicine.diseaseCytokinemedicine.anatomical_structureImmunologyCytokinesInterleukin-2Tumor necrosis factor alphamedicine.drugImmunologic research
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Transcriptional regulation of miR-224 upregulated in human HCCs by NFκB inflammatory pathways

2012

Background & Aims: miR-224 is up-regulated in human HCCs as compared to both paired peri-tumoral cirrhotic tissues and cirrhotic livers without HCC. Here, we have cloned the miR-224 regulatory region and characterized its transcriptional regulation by the NFκB-dependent inflammatory pathways. Methods: Mature miRNA expression was evaluated by a 2 step stem-loop real-time RT-PCR. The recruitment of polymerase II and transcription factors on the pre-miR-224 promoter has been assessed by ChIPSeq and ChIP. Results: We found miR-224 levels strongly up-regulated in both peri-tumoral cirrhotic livers and HCC samples as compared to normal livers. In silico analysis of the putative miR-224 promoter r…

LipopolysaccharidesLiver CirrhosisMaleCarcinoma HepatocellularTranscription GeneticLiver CirrhosiLipopolysaccharideBiologyCell MovementCell Line TumormicroRNATranscriptional regulationHumansNF kappa BHCCmir-224; nfκb; hcc; mirnas; transcriptionTranscription factorLymphotoxin-alphamiRNAAgedHepatologymiRNAs; HCC; miR-224; Transcription; NF kappa BTumor Necrosis Factor-alphaLiver NeoplasmsNF-kappa BMicroRNAmiR-224HCCSMiddle AgedNFKB1Up-RegulationMicroRNAsIκBαLiverLiver NeoplasmCase-Control StudiesImmunologymiRNAsCancer researchTumor necrosis factor alphaFemaleSignal transductionCase-Control StudieTranscriptionNFκBHumanSignal Transduction
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mTORC1 activation in B cells confers impairment of marginal zone microarchitecture by exaggerating cathepsin activity

2018

Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell metabolism and lymphocyte proliferation. It is inhibited by the tuberous sclerosis complex (TSC), a heterodimer of TSC1 and TSC2. Deletion of either gene results in robust activation of mTORC1. Mature B cells reside in the spleen at two major anatomical locations, the marginal zone (MZ) and follicles. The MZ constitutes the first line of humoral response against blood‐borne pathogens and undergoes atrophy in chronic inflammation. In previous work, we showed that mice deleted for TSC1 in their B cells (TSC1(BKO)) have almost no MZ B cells, whereas follicular B cells are minimally affected. To explore potential underl…

Lymphotoxin-beta0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesImmunologyMice TransgenicSpleenCHO CellsmTORC1Lymphocyte proliferationMechanistic Target of Rapamycin Complex 1Tuberous Sclerosis Complex 1 ProteinCathepsin BCell LineMice03 medical and health sciencesCricetulus0302 clinical medicineLymphotoxin beta ReceptorTuberous Sclerosis Complex 2 ProteinmedicineAnimalsImmunology and AllergyReceptorLymphotoxin-alphaSirolimusCathepsinB-LymphocytesChemistryOriginal ArticlesMarginal zoneCathepsinsCell biology030104 developmental biologymedicine.anatomical_structureLymphotoxinSpleen030215 immunologyImmunology
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Tumor necrosis factor (TNF) and lymphotoxin-a (LTA) polymorphisms and risk of non-hodgkin lymphoma in the interLymph consortium

2010

In an International Lymphoma Epidemiology Consortium pooled analysis, polymorphisms in 2 immune-system-related genes, tumor necrosis factor (TNF) and interleukin-10 (IL10), were associated with non-Hodgkin lymphoma (NHL) risk. Here, 8,847 participants were added to previous data (patients diagnosed from 1989 to 2005 in 14 case-control studies; 7,999 cases, 8,452 controls) for testing of polymorphisms in the TNF -308G>A (rs1800629), lymphotoxin-alpha (LTA) 252A>G (rs909253), IL10 -3575T>A (rs1800890, rs1800896), and nucleotide-binding oligomerization domain containing 2 (NOD2) 3020insC (rs2066847) genes. Odds ratios were estimated for non-Hispanic whites and several ethnic subgroups using 2-…

MaleEpidemiologyTNFGastroenterology0302 clinical medicineRisk Factorsimmune system diseaseshemic and lymphatic diseasesAged 80 and over0303 health scienceseducation.field_of_studyLymphoma Non-Hodgkinnon-Hodgkin lymphomaMiddle Aged3. Good healthInterleukin-10EuropeLTA030220 oncology & carcinogenesisFemaleLymphotoxin alphaAdultmedicine.medical_specialtyCanadaAdolescentTumor necrosis factorMeta- and Pooled AnalysesPopulationPolymorphism Single NucleotideWhite People03 medical and health sciencesYoung AdultInternal medicinemedicineHumansGenetic Predisposition to Diseaseeducation030304 developmental biologyAgedMycosis fungoidesbusiness.industryTumor Necrosis Factor-alphaAustraliaInternational AgenciesInterLymph ConsortiumOdds ratiomedicine.diseaseUnited StatesNon-Hodgkin's lymphomaLymphomaCase-Control StudiesImmunologyMantle cell lymphomalymphotoxin-alphabusinessDiffuse large B-cell lymphoma
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Soluble interleukin-6 receptor (sIL-6R) makes IL-6R negative T cell line respond to IL-6: it inhibits TNF production

2000

The receptor for interleukin-6 (IL-6) consists of two subunits: a ligand specific IL-6Ralpha and gp130 that is responsible for signal-transduction. A soluble form of the ligand specific chain was described that when complexed to IL-6 is capable of binding to the membrane-bound gp130 subunit and thus can elicit signal-transduction. This soluble receptor can act on cells that express only the gp130 but not the ligand-specific subunit of the IL-6R. This phenomenon, called trans-signaling, introduced a novel aspect of cytokine action. In this study we examined the response of Jurkat cells, that are known not to express IL-6Ralpha, to IL-6, the soluble IL-6 receptor (sIL-6R) and a covalent compl…

Recombinant Fusion ProteinsT-Lymphocytesmedicine.medical_treatmentT cellImmunologyBiologyJurkat cellsCell LineInterferon-gammaJurkat CellsAntigens CDCytokine Receptor gp130medicineHumansImmunology and AllergyInterferon gammaElméleti orvostudományokReceptorLymphotoxin-alphaMembrane GlycoproteinsInterleukin-6Tumor Necrosis Factor-alphaReceptors InterleukinOrvostudományokLigand (biochemistry)Glycoprotein 130Receptors Interleukin-6Molecular biologyCytokinemedicine.anatomical_structureSolubilityTumor necrosis factor alphamedicine.drug
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Differential regulation of interleukin-6 expression in human fibroblasts by tumor necrosis factor-alpha and lymphotoxin.

1990

The treatment of human diploid fibroblasts with tumor necrosis factor (TNF)-alpha and with lymphotoxin (LT) is associated with induction of interleukin-6 (IL-6) transcripts with TNF-alpha being 10-fold more potent than LT. Here we report on the TNF-alpha/LT-induced signaling mechanisms responsible for the regulation of IL-6 gene expression in these cells. Run-on assays demonstrated that both TNF-alpha and LT increase IL-6 mRNA levels by transcriptional activation of this gene. Stability studies of IL-6 transcripts in fibroblasts showed that TNF-alpha delayed IL-6 mRNA decay but not LT. The induction of IL-6 transcripts by TNF-alpha and LT was not inhibited by the isoquinoline sulfonamide de…

medicine.medical_specialtyTime FactorsTranscription Geneticmedicine.medical_treatmentCellular differentiationBiophysicsCycloheximideBiologyBiochemistrychemistry.chemical_compoundStructural BiologyInternal medicineGene expressionGeneticsmedicineHumansRNA MessengerMolecular BiologyLymphotoxin-alphaProtein kinase CCells CulturedProtein Kinase CInterleukin-6Tumor Necrosis Factor-alphaCell BiologyFibroblastsMolecular biologyKineticsCytokineLymphotoxinEndocrinologychemistryGene Expression RegulationProtein BiosynthesisTumor necrosis factor alphaSignal transductionFEBS letters
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