Search results for "T cell"

showing 10 items of 2228 documents

The astrocyte LAMP lights a T cell TRAIL of death

2021

In a recent issue of Nature, Sanmarco et al. reveal a novel mechanism by which astrocytes maintain an anti-inflammatory state in the central nervous system (CNS). IFNγ released by gut-licensed meningeal NK cells was found to induce TRAIL expression on astrocytes, causing effector T cell apoptosis.

0301 basic medicineEffectorGeneral NeuroscienceT cellCentral nervous systemBiologyCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicine030217 neurology & neurosurgeryAstrocyteNeuron
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Sema3a plays a role in the pathogenesis of CHARGE syndrome

2018

CHARGE syndrome is an autosomal dominant malformation disorder caused by heterozygous loss of function mutations in the chromatin remodeler CHD7. Chd7 regulates the expression of Sema3a, which also contributes to the pathogenesis of Kallmann syndrome, a heterogeneous condition with the typical features hypogonadotropic hypogonadism and an impaired sense of smell. Both features are common in CHARGE syndrome suggesting that SEMA3A may provide a genetic link between these syndromes. Indeed, we find evidence that SEMA3A plays a role in the pathogenesis of CHARGE syndrome. First, Chd7 is enriched at the Sema3a promotor in neural crest cells and loss of function of Chd7 inhibits Sema3a expression…

0301 basic medicineEmbryo NonmammalianKallmann syndromePHENOTYPIC SPECTRUMmedicine.disease_causeSeverity of Illness IndexEpigenesis GeneticPathogenesisAXON GUIDANCECHD7CHARGE syndromeXenopus laevis0302 clinical medicineHYPOGONADOTROPIC HYPOGONADISMPromoter Regions GeneticGenetics (clinical)GeneticsMutationGeneral MedicinePhenotypeDNA-Binding ProteinsNEURAL CREST CELLSNeural CrestHomeobox Protein Nkx-2.5MIGRATIONBiology03 medical and health sciencesHypogonadotropic hypogonadismKALLMANN-SYNDROMEGeneticsmedicineAnimalsHumansEpigeneticsSHORT STATUREMolecular BiologyLoss functionMUTATIONSGenetic Complementation TestDNA HelicasesSemaphorin-3AKallmann Syndromemedicine.diseaseDisease Models Animal030104 developmental biologyHEK293 CellsXENOPUS-EMBRYOSMutationCHARGE Syndrome030217 neurology & neurosurgery
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Nickel toxicity in P. lividus embryos: Dose dependent effects and gene expression analysis.

2018

Abstract Many industrial activities release Nickel (Ni) in the environment with harmful effects for terrestrial and marine organisms. Despite many studies on the mechanisms of Ni toxicity are available, the understanding about its toxic effects on marine organisms is more limited. We used Paracentrotus lividus as a model to analyze the effects on the stress pathways in embryos continuously exposed to different Ni doses, ranging from 0.03 to 0.5 mM. We deeply examined the altered embryonic morphologies at 24 and 48 h after Ni exposure. Some different phenotypes have been classified, showing alterations at the expenses of the dorso-ventral axis as well as the skeleton and/or the pigment cells…

0301 basic medicineEmbryo NonmammalianPigment cellmRNASettore BIO/05 - ZoologiaEmbryonic DevelopmentGene ExpressionDevelopmentAquatic ScienceOceanographyParacentrotus lividus03 medical and health sciencesNickelGene expressionAnimalsInvertebrateProtein kinase AGeneSkeletonEchinodermbiologyAnimalChemistryStress responseEmbryoGeneral Medicinebiology.organism_classificationPollutionPhenotypeCell biologyHeavy metal030104 developmental biologyToxicityUnfolded protein responseParacentrotusParacentrotuWater Pollutants ChemicalMarine environmental research
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IL ‐1 signaling is critical for expansion but not generation of autoreactive GM ‐ CSF + Th17 cells

2016

Abstract Interleukin‐1 (IL‐1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL‐1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL‐1 receptor type 1 (IL‐1R1)‐dependent IL‐1β expression by myeloid cells in the draining lymph nodes. This myeloid‐derived IL‐1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM‐CSF + Th17 cell subset, thereby enhancing its encephalitog…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalBiologymedicine.disease_causePertussis toxinGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityMice03 medical and health sciences0302 clinical medicineMediatormedicineAnimalsInducerMolecular BiologyCell ProliferationGeneral Immunology and MicrobiologyGeneral NeuroscienceMultiple sclerosisExperimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorArticlesmedicine.diseaseCell biology030104 developmental biologyPertussis ToxinT cell subsetImmunologyTh17 CellsLymphInterleukin-1030215 immunologyThe EMBO Journal
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Gatekeeper role of brain antigen‐presenting CD11c + cells in neuroinflammation

2015

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesAntigen-Presenting CellsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInterleukin 210302 clinical medicineCell MovementAnimalsCytotoxic T cellAntigen-presenting cellMolecular BiologyNeuroinflammationInterleukin 3CD40General Immunology and MicrobiologybiologyGeneral NeuroscienceInterleukin-17BrainGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsDendritic CellsArticlesNatural killer T cellCD11c AntigenMice Inbred C57BL030104 developmental biologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunologyThe EMBO Journal
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T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita

2016

AbstractT cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to the effector phase of antibody-mediated autoimmune dermatoses, i.e., tissue injury and inflammation of the skin, has not been investigated. In this paper, we demonstrate that T cells amplify the development of autoantibody-induced tissue injury in a prototypical, organ-specific autoimmune disease, namely epidermolysis bullosa acquisita (EBA) – characterized and caused by autoantibodies targeting type VII collagen. Specifically, we show that immune complex (IC)-induced inflammation depends on the presence of T cells – a process facilitated by T cell receptor (…

0301 basic medicineEpidermolysis bullosa acquisitamedicine.medical_specialtyCollagen Type VIINeutrophilsT-LymphocytesGene ExpressionMice NudeInflammationAntigen-Antibody ComplexCell CommunicationEpidermolysis Bullosa AcquisitaArticleMice03 medical and health sciencesCricetulus0302 clinical medicinemedicineAnimalsHumansAutoantibodiesSkinAutoimmune diseaseMice Inbred BALB CMultidisciplinarybusiness.industryT-cell receptorAutoantibodyAntibodies MonoclonalReceptors Antigen T-Cell gamma-deltamedicine.diseaseNatural killer T cellDermatologyImmune complexMice Inbred C57BLDisease Models Animal030104 developmental biologyLymphatic systemImmunoglobulin GImmunologyNatural Killer T-CellsLymph NodesRabbitsmedicine.symptombusinessSpleenSignal Transduction030215 immunologyScientific Reports
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Population snapshots predict early haematopoietic and erythroid hierarchies

2016

The formation of red blood cells begins with the differentiation of multipotent haematopoietic progenitors. Reconstructing the steps of this differentiation represents a general challenge in stem-cell biology. Here we used single-cell transcriptomics, fate assays and a theory that allows the prediction of cell fates from population snapshots to demonstrate that mouse haematopoietic progenitors differentiate through a continuous, hierarchical structure into seven blood lineages. We uncovered coupling between the erythroid and the basophil or mast cell fates, a global haematopoietic response to erythroid stress and novel growth factor receptors that regulate erythropoiesis. We defined a flow …

0301 basic medicineErythrocytesPopulationBiologyArticleTranscriptomeMice03 medical and health sciencesSingle-cell analysisRNA Small CytoplasmicAnimalsCell LineageErythropoiesisMast CellsProgenitor celleducationProgenitorErythroid Precursor Cellseducation.field_of_studyMultidisciplinaryCell CycleCell cycleFlow CytometryBasophilsCell biologyProto-Oncogene Proteins c-kitHaematopoiesis030104 developmental biologyIntercellular Signaling Peptides and ProteinsErythropoiesisFemaleSingle-Cell AnalysisTranscriptomeNature
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Anthranilamide-based 2-phenylcyclopropane-1-carboxamides, 1,1'-biphenyl-4-carboxamides and 1,1'-biphenyl-2-carboxamides: Synthesis biological evaluat…

2017

Abstract Several anthranilamide-based 2-phenylcyclopropane-1-carboxamides 13a-f, 1,1’-biphenyl-4-carboxamides 14a-f and 1,1’-biphenyl-2-carboxamides 17a-f were obtained by a multistep procedure starting from the (1S,2S)-2-phenylcyclopropane-1-carbonyl chloride 11, the 1,1'-biphenyl-4-carbonyl chloride 12 or the 1,1'-biphenyl-2-carbonyl chloride 16 with the appropriate anthranilamide derivative 10a-f. Derivatives 13a-f, 14a-f and 17a-f showed antiproliferative activity against human leukemia K562 cells. Among these derivatives 13b, 14b and 17b exerted a particular cytotoxic effect on tumor cells. Derivative 17b showed a better antitumoral effect on K562 cells than 13b and 14b. Analyses perfo…

0301 basic medicineG2 Phase2-Phenylcyclopropane-1-carboxamides 11’-biphenyl-4-carboxamides 11’-biphenyl-2-carboxamides G2/M arrest Phospho-ATM and gH2AX increaseDNA RepairDNA repairStereochemistryAntineoplastic AgentsApoptosisChloride03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaDrug DiscoverymedicineCytotoxic T cellHumansortho-AminobenzoatesMode of actionCell ProliferationPharmacologyChemistryOrganic ChemistryGeneral MedicineCell Cycle CheckpointsCell cycleSettore CHIM/08 - Chimica Farmaceutica030104 developmental biologyMechanism of actionApoptosis030220 oncology & carcinogenesismedicine.symptomK562 CellsDNAmedicine.drugDNA Damage
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Ectopic expression of CXCL13, BAFF, APRIL and LT-ß is associated with artery tertiary lymphoid organs in giant cell arteritis

2016

ObjectivesTo investigate whether artery tertiary lymphoid organs (ATLOs) are present in giant cell arteritis (GCA) and that their formation is associated with the ectopic expression of constitutive lymphoid tissue-homing chemokines.MethodsReverse transcriptase PCR, immunohistochemical and immunofluorescence analysis were used to determine the presence of ectopic ATLOs in GCA and the expression of chemokines/chemokine receptors and cytokines involved in lymphoneogenesis in the temporal artery samples obtained from 50 patients with GCA and 30 controls. The presence of lymphatic conduits, of follicular dendritic cells (FDCs) precursors and lymphoid tissue inducer cells was also investigated. F…

0301 basic medicineGenetics and Molecular Biology (all)ChemokineChemokines; Cytokines; Giant Cell Arteritis; Rheumatology; Immunology; Biochemistry Genetics and Molecular Biology (all); Immunology and AllergyHigh endothelial venulesImmunologyBiologyBiochemistryGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesChemokine receptor0302 clinical medicineRheumatologyChemokines; Cytokines; Giant Cell ArteritisImmunology and AllergyCXCL13B-cell activating factorCytokineGiant Cell Arteriti030203 arthritis & rheumatologyBiochemistry Genetics and Molecular Biology (all)Follicular dendritic cellsSettore MED/16 - Reumatologia030104 developmental biologyLymphatic systemChemokineImmunologybiology.proteinEctopic expression
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Response to: 'Artery tertiary lymphoid organs in giant cell arteritis are not exclusively located in the media of temporal arteries' by Graver et al

2017

We thank Graver  et al 1 for their interest in our recently published article on artery tertiary lymphoid organs (ATLOs) in giant cell arteritis (GCA).2 The authors stained temporal artery biopsies of 21 biopsy-proven GCA patients (71% female, mean duration of disease of 2.3±0.9 months) that fulfilled the 1990 American College of Rheumatology classification criteria with anti-CD20 and anti-CD3 antibodies. On the basis of this experimental approach, they confirmed the presence of ATLOs only in the adventitia of inflamed arteries of GCA patients and not in the media as demonstrated in our study. This statement, however, is not supported in our opinion by the experimental approach chosen …

0301 basic medicineGenetics and Molecular Biology (all)medicine.medical_specialtyPathologyBiopsyGiant Cell ArteritisImmunologyDisease Activity; Giant Cell Arteritis; TreatmentBiochemistryGeneral Biochemistry Genetics and Molecular BiologyDisease activity03 medical and health sciences0302 clinical medicineRheumatologyInternal medicineAdventitiamedicineHumansImmunology and AllergyDisease ActivityGiant Cell Arteriti030203 arthritis & rheumatologyBiochemistry Genetics and Molecular Biology (all)business.industryArteriesmedicine.diseaseRheumatologyTemporal ArteriesTreatmentGiant cell arteritis030104 developmental biologymedicine.anatomical_structureLymphatic systemcardiovascular systemTemporal arterybusinessArtery
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