Search results for "R Factors"

showing 10 items of 39 documents

Regulatory T cells--the renaissance of the suppressor T cells.

2007

Immune reactions are stringently regulated and balanced by complex interactions of stimulating and suppressing mechanisms. Dysfunctions of this sophisticated immune regulatory network can lead to a variety of diseases such as autoimmunity, allergy, cancer, and pregnancy disorders. The rediscovery of suppressor T cells a decade ago--now designated as T regulatory cells--set off a huge avalanche of research activities leading to a multitude of preclinical and clinical studies. Herein, we give a comprehensive review about this research on T regulatory cells and the relevance of this suppressive T cell population for the development of innovative immune therapeutic strategies.

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentT cellPopulationAutoimmunitymedicine.disease_causeInfectionsT-Lymphocytes RegulatoryAutoimmunitylaw.inventionMiceImmune systemlawPregnancyT-Lymphocyte SubsetsTransplantation ImmunologyNeoplasmsmedicineSuppressor Factors ImmunologicAnimalsHumanseducationeducation.field_of_studybusiness.industryModels ImmunologicalGeneral MedicineT lymphocyteImmunotherapyInflammatory Bowel DiseasesTransplantationDisease Models Animalmedicine.anatomical_structureDiabetes Mellitus Type 1ImmunologySuppressorFemaleImmunotherapybusinessAnnals of medicine
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Logarithmic Equal-Letter Runs for BWT of Purely Morphic Words

2022

In this paper we study the number r(bwt) of equal-letter runs produced by the Burrows-Wheeler transform (BWT) when it is applied to purely morphic finite words, which are words generated by iterating prolongable morphisms. Such a parameter r(bwt) is very significant since it provides a measure of the performances of the BWT, in terms of both compressibility and indexing. In particular, we prove that, when BWT is applied to whichever purely morphic finite word on a binary alphabet, r(bwt) is O(log n), where n is the length of the word. Moreover, we prove that r(bwt) is Theta(log n) for the binary words generated by a large class of prolongable binary morphisms. These bounds are proved by pro…

Equal-letter runsSettore INF/01 - InformaticaMorphismsBurrows-Wheeler TransformBispecial circular factors
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Immunochemical analysis of the carbohydrate moiety of yeast killer toxin K28

1990

Killer toxin K28, a 16 kd protein secreted by the wine yeast Saccharomyces cerevisiae strain 28, was reversibly bound by a column of Concanavalin A-Sepharose, confirming its glycoprotein nature. HPLC analysis of acid hydrolyzates of K28 toxin as well as Western-blots of beta-eliminated and/or endo H-treated killer toxin preparations probed with polyclonal alpha-toxin antibodies revealed that the carbohydrate moiety of K28 consists of D-mannose only, which is O-glycosidically linked via Ser/Thr residues to the protein part. The change in gel mobility of K28 after beta-elimination was caused by a decrease in molecular mass of about 1,800, corresponding to a carbohydrate moiety of 10 mannose r…

GlycosylationSaccharomyces cerevisiae ProteinsGlycosylationBlotting WesternSaccharomyces cerevisiaeMannoseSaccharomyces cerevisiaemedicine.disease_causeMicrobiologyChromatography Affinitychemistry.chemical_compoundmedicineMolecular BiologyAntibodies FungalChromatography High Pressure Liquidchemistry.chemical_classificationbiologyMolecular massToxinImmunochemistrySepharoseGeneral MedicineMycotoxinsbiology.organism_classificationKiller Factors YeastYeastchemistryBiochemistryPolyclonal antibodiesbiology.proteinGlycoproteinMannoseAntonie van Leeuwenhoek
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Killer toxin of Hanseniaspora uvarum

1990

The yeast Hanseniaspora uvarum liberates a killer toxin lethal to sensitive strains of the species Saccharomyces cerevisiae. Secretion of this killer toxin was inhibited by tunicamycin, an inhibitor of N-glycosylation, although the mature killer protein did not show any detectable carbohydrate structures. Culture supernatants of the killer strain were concentrated by ultrafiltration and the extracellular killer toxin was precipitated with ethanol and purified by ion exchange chromatography. SDS-PAGE of the electrophoretically homogenous killer protein indicated an apparent molecular mass of 18,000. Additional investigations of the primary toxin binding sites within the cell wall of sensitiv…

GlycosylationSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaechemical and pharmacologic phenomenaSaccharomyces cerevisiaemedicine.disease_causeHanseniasporaBiochemistryMicrobiologyMicrobiologyFungal Proteinschemistry.chemical_compoundCell WallGeneticsmedicineExtracellularSecretionIsoelectric PointGlucansMolecular BiologyBinding SitesbiologyMolecular massToxinGeneral MedicineTunicamycinMycotoxinsChromatography Ion Exchangebiology.organism_classificationKiller Factors YeastYeastBiochemistrychemistrySaccharomycetalesElectrophoresis Polyacrylamide GelArchives of Microbiology
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CCAAT/Enhancer-binding Protein α (C/EBPα) and Hepatocyte Nuclear Factor 4α (HNF4α) Synergistically Cooperate with Constitutive Androstane Receptor to…

2010

The transcription of tissue-specific and inducible genes is usually subject to the dynamic control of multiple activators. Dedifferentiated hepatic cell lines lose the expression of tissue-specific activators and many characteristic hepatic genes, such as drug-metabolizing cytochrome P450. Here we demonstrate that by combining adenoviral vectors for CCAAT/enhancer-binding protein α (C/EBPα), hepatocyte nuclear factor 4α (HNF4α), and constitutive androstane receptor, the CYP2B6 expression and inducibility by CITCO are restored in human hepatoma HepG2 cells at levels similar to those in cultured human hepatocytes. Moreover, several other phase I and II genes are simultaneously activated, whic…

Hepatocyte nuclear factorsCcaat-enhancer-binding proteinsTranscription (biology)Hepatocyte nuclear factor 4 alphaConstitutive androstane receptorTranscriptional regulationCell BiologyBiologyReceptorMolecular BiologyBiochemistryTranscription factorMolecular biologyJournal of Biological Chemistry
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Uremic serum inhibits monocyte-dependent, but not interleukin-2-dependent steps of T cell proliferation.

1990

We examined the influence of uremic serum on antigen receptor triggered T cell proliferation in dialysis patients with impaired immune function, i.e., 12 nonresponders to hepatitis B vaccination. The dialysis patients showed a monocyte dysfunction and an increased responsiveness to interleukin 2 (IL-2) according to our previous findings. In vitro the addition of IL-2 completely reconstituted the defect. Uremic serum inhibited monocyte-dependent T cell proliferation of patients and of healthy controls. Contrary, monocyte-independent steps of T cell proliferation were not impaired by uremic serum. When IL-2 was added to cultures, the T cell proliferation in the presence of uremic serum was ev…

Interleukin 2AdultMalemedicine.medical_specialtyT cellT-LymphocytesLymphocyte ActivationMonocytesImmune toleranceImmune systemInternal medicinemedicineImmune ToleranceSuppressor Factors ImmunologicHumansAgedUremiabusiness.industryCell growthMonocyteT lymphocyteMiddle Agedmedicine.diseaseUremiamedicine.anatomical_structureEndocrinologyInterleukin-2businessmedicine.drugNephron
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Cyclic adenosine monophosphate is a key component of regulatory T cell–mediated suppression

2007

Naturally occurring regulatory T cells (T reg cells) are a thymus-derived subset of T cells, which are crucial for the maintenance of peripheral tolerance by controlling potentially autoreactive T cells. However, the underlying molecular mechanisms of this strictly cell contact–dependent process are still elusive. Here we show that naturally occurring T reg cells harbor high levels of cyclic adenosine monophosphate (cAMP). This second messenger is known to be a potent inhibitor of proliferation and interleukin 2 synthesis in T cells. Upon coactivation with naturally occurring T reg cells the cAMP content of responder T cells is also strongly increased. Furthermore, we demonstrate that natur…

Interleukin 2CD4-Positive T-LymphocytesMaleRegulatory T cellImmunologyEnzyme-Linked Immunosorbent AssayBiologySecond Messenger SystemsT-Lymphocytes RegulatoryConnexinschemistry.chemical_compoundMiceImmune systemmedicineCyclic AMPSuppressor Factors ImmunologicImmunology and AllergyAnimalsCyclic adenosine monophosphateIL-2 receptorDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionZAP70Intercellular transportBrief Definitive ReportPeripheral toleranceGap JunctionsMolecular biologyMice Inbred C57BLmedicine.anatomical_structurechemistryBrief Definitive ReportsCytokinesFemaleOligopeptidesmedicine.drugThe Journal of Experimental Medicine
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Production of T suppressor factor specific for the hapten picryl chloride requires both T suppressor cells and an antigen-specific, genetically restr…

1987

Summary We investigated the requirement for activation of T suppressor cells specific for the hapten picryl chloride and the release of hapten-specific T suppressor factor. Using an in vivo experimental system, we report that activation of T suppressor cells and the consequent release of T suppressor factor required two signals: one was provided by primed T suppressor cells, i.e. spleen cells from mice injected with the tolerogen picrylsulphonic acid, and the other was provided by the specific antigen in the context of H-2 gene products. Mechanisms by which the interaction between these two signals led to activation of T suppressor cells and the production of T suppressor factor, as well as…

MaleMice Inbred StrainsPicryl ChlorideBiologyT-Lymphocytes Regulatorylaw.inventionPicryl chlorideEpitopesMicechemistry.chemical_compoundInterleukin 21AntigenlawSuppressor Factors ImmunologicAnimalsCytotoxic T cellDisulfidesCells CulturedGeneral Environmental ScienceH-2 AntigensLymphokineGeneral MedicineT lymphocyteCell biologychemistryImmunologyGeneral Earth and Planetary SciencesSuppressorFemaleHaptensOxidation-ReductionHaptenSpleenAnnales de l'Institut Pasteur / Immunologie
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Transcriptional activation of CYP2C9, CYP1A1, and CYP1A2 by hepatocyte nuclear factor 4alpha requires coactivators peroxisomal proliferator activated…

2006

Hepatocyte nuclear factor 4alpha (HNF4alpha) is a key transcription factor for the constitutive expression of cytochromes P450 (P450s) in the liver. However, human hepatoma HepG2 cells show a high level of HNF4alpha but express only marginal P450 levels. We found that the HNF4alpha-mediated P450 transcription in HepG2 is impaired by the low level of coactivators peroxisomal proliferator activated receptor-gamma coactivator 1alpha (PGC1alpha) and steroid receptor coactivator 1 (SRC1). Reporter assays with a chimeric CYP2C9-LUC construct demonstrated that the sole transfection of coactivators induced luciferase activity in HepG2 cells. In HeLa cells however, CYP2C9-LUC activity only significa…

MaleTranscriptional Activationendocrine systemBiologyResponse ElementsTransfectiondigestive systemAdenoviridaeNuclear Receptor Coactivator 1Cytochrome P-450 CYP1A2CoactivatorCytochrome P-450 CYP1A1HumansInsulinTranscription factorCells CulturedHeat-Shock ProteinsCytochrome P-450 CYP2C9Histone AcetyltransferasesPharmacologyTransfectionMiddle AgedMolecular biologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaNuclear receptor coactivator 1Hepatocyte nuclear factorsHepatocyte Nuclear Factor 4Nuclear receptor coactivator 3Nuclear receptor coactivator 2HepatocytesMolecular MedicineFemaleAryl Hydrocarbon HydroxylasesChromatin immunoprecipitationHeLa CellsProtein BindingTranscription FactorsMolecular pharmacology
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Killer-toxin-resistant kre12 mutants of Saccharomyces cerevisiae: genetic and biochemical evidence for a secondary K1 membrane receptor.

1995

The Saccharomyces cerevisiae killer toxin K1 is a secreted alpha/beta-heterodimeric protein toxin that kills sensitive yeast cells in a receptor-mediated two-stage process. The first step involves toxin binding to beta-1,6-D-glucan-components of the outer yeast cell surface; this step is blocked in yeast mutants bearing nuclear mutations in any of the KRE genes whose products are involved in synthesis and/or assembly of cell wall beta-D-glucans. After binding to the yeast cell wall, the killer toxin is transferred to the cytoplasmic membrane, subsequently leading to cell death by forming lethal ion channels. In an attempt to identify a secondary K1 toxin receptor at the plasma membrane leve…

MutantSaccharomyces cerevisiaeGenes FungalReceptors Cell SurfaceSaccharomyces cerevisiaeSpheroplastsBiologymedicine.disease_causeBiochemistryMicrobiologyModels BiologicalIon ChannelsFungal ProteinsCell surface receptorCell WallGeneticsmedicineMolecular BiologyDiphtheria toxinToxinMembrane ProteinsDrug Resistance MicrobialGeneral MedicineSpheroplastMycotoxinsbiology.organism_classificationYeastKiller Factors YeastBiochemistryMembrane proteinMutationArchives of microbiology
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