Search results for "IL3"

showing 5 items of 5 documents

E4BP4/NFIL3 modulates the epigenetically repressed RAS effector RASSF8 function through histone methyltransferases

2018

RAS proteins are major human oncogenes, and most of the studies are focused on enzymatic RAS effectors. Recently, nonenzymatic RAS effectors (RASSF, RAS association domain family) have garnered special attention because of their tumor-suppressive properties in contrast to the oncogenic potential of the classical enzymatic RAS effectors. Whereas most members of RASSF family are deregulated by promoter hypermethylation, RASSF8 promoter remains unmethylated in many cancers but the mechanism(s) of its down-regulation remains unknown. Here, we unveil E4BP4 as a critical transcriptional modulator repressing RASSF8 expression through histone methyltransferases, G9a and SUV39H1. In line with these …

0301 basic medicineTumor suppressor geneBreast NeoplasmsBiologyBiochemistryEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistocompatibility AntigensHistone methylationHumansEpigeneticsMolecular BiologySUV39H1EffectorTumor Suppressor ProteinsNFIL3Molecular Bases of DiseaseCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesCell biologyNeoplasm ProteinsGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyBasic-Leucine Zipper Transcription FactorsHEK293 Cells030220 oncology & carcinogenesisHistone methyltransferaseMCF-7 CellsFemaleFunction (biology)
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Differentiation of Type 1 ILCs from a Common Progenitor to All Helper-like Innate Lymphoid Cell Lineages

2014

SummaryInnate lymphoid cells (ILCs) are a recently recognized group of lymphocytes that have important functions in protecting epithelial barriers against infections and in maintaining organ homeostasis. ILCs have been categorized into three distinct groups, transcriptional circuitry and effector functions of which strikingly resemble the various T helper cell subsets. Here, we identify a common, Id2-expressing progenitor to all interleukin 7 receptor-expressing, “helper-like” ILC lineages, the CHILP. Interestingly, the CHILP differentiated into ILC2 and ILC3 lineages, but not into conventional natural killer (cNK) cells that have been considered an ILC1 subset. Instead, the CHILP gave rise…

Cellular differentiationLineage (evolution)Bone Marrow CellsGATA3 Transcription FactorBiologyGeneral Biochemistry Genetics and Molecular BiologyMicemedicineAnimalsLymphocytesskin and connective tissue diseasesProgenitorInhibitor of Differentiation Protein 2Receptors Interleukin-7Biochemistry Genetics and Molecular Biology(all)Intracellular parasiteStem CellsInnate lymphoid cellNFIL3Cell DifferentiationT helper cellImmunity InnateMice Inbred C57BLbody regionsmedicine.anatomical_structureImmunologyToxoplasmaIntracellularToxoplasmosisCell
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Type I Interferon Protects Antiviral CD8+ T Cells from NK Cell Cytotoxicity

2014

Summary Despite development of new antiviral drugs, viral infections are still a major health problem. The most potent antiviral defense mechanism is the innate production of type I interferon (IFN-I), which not only limits virus replication but also promotes antiviral T cell immunity through mechanisms, which remain insufficiently studied. Using the murine lymphocytic choriomeningitis virus model system, we show here that IFN-I signaling on T cells prevented their rapid elimination in vivo. Microarray analyses uncovered that IFN-I triggered the expression of selected inhibitory NK-cell-receptor ligands. Consequently, T cell immunity of IFN-I receptor (IFNAR)-deficient T cells could be rest…

Cytotoxicity ImmunologicImmunologyMedizinReceptor Interferon alpha-betaCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisVirus ReplicationLymphocytic choriomeningitisVirusMiceImmunityInterferonmedicineAnimalsLymphocytic choriomeningitis virusImmunology and AllergyCytotoxic T cellCells CulturedMice KnockoutbiologyPerforinNFIL3medicine.diseaseVirologyImmunity InnateKiller Cells NaturalMice Inbred C57BLBasic-Leucine Zipper Transcription FactorsInfectious DiseasesViral replicationPerforinInterferon Type IImmunologybiology.proteinSignal Transductionmedicine.drugImmunity
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Esosomi ingegnerizzati per il trattamento della leucemia mieloide cronica

2016

La presente invenzione si riferisce al settore delle biotecnologie e più in particolare a quello dell’ingegneria genetica in quanto fornisce vescicole esosomiali ingegnerizzate affinché esprimano una specifica proteina di fusione che li rende adatti come veicolanti, sito e cellula specifici, di principi attivi nei confronti delle cellule il cui processo proliferativo risulta alterato e che sono coinvolte nella patogenesi della leucemia mieloide cronica.

IL3leucemia mieloide cronicaesosomi
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Interleukin-36α axis is modulated in patients with primary Sjögren's syndrome.

2015

Summary The aim of this study was to investigate the expression of the interleukin (IL)-36 axis in patients with primary Sjögren's syndrome (pSS). Blood and minor labial salivary glands (MSG) biopsies were obtained from 35 pSS and 20 non-Sjögren's syndrome patients (nSS) patients. Serum IL-36α was assayed by enzyme-linked immunosorbent assay (ELISA). IL-36α, IL-36R, IL-36RA, IL-38, IL-22, IL-17, IL-23p19 and expression in MSGs was assessed by reverse transcription–polymerase chain reaction (RT–PCR), and tissue IL-36α and IL-38 expression was also investigated by immunohistochemistry (IHC). αβ and γδ T cells and CD68+ cells isolated from MSGs were also studied by flow cytometry and confocal …

MaleReceptors Antigen T-Cell alpha-betaT-LymphocytesSalivary GlandsIL-36aIL-36a IL-38 IL36RA Sjogren's syndrome γδT cellsImmunology and AllergyMedicinemedicine.diagnostic_testSalivary glandbiologyCD68γδT cellsInterleukin-17TranslationalIL-36a; IL-38; IL36RA; Sjögren's syndrome; γδ T cellsInterleukinReceptors Antigen T-Cell gamma-deltaMiddle Agedmedicine.anatomical_structureSjogren's SyndromeImmunohistochemistryFemaleSjögren's syndromeInterleukin 17Signal TransductionAdultmedicine.medical_specialtyCD3ImmunologyPrimary Cell CultureAntigens Differentiation Myelomonocyticγδ T cellsIL36RAFlow cytometrystomatognathic systemAntigens CDInternal medicineHumansbusiness.industryInterleukinsReceptors InterleukinIL-38stomatognathic diseasesSettore MED/16 - ReumatologiaEndocrinologyGene Expression RegulationCell cultureCase-Control StudiesImmunologybiology.proteinInterleukin-23 Subunit p19businessInterleukin-1
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