Search results for " Cell"

showing 10 items of 14074 documents

Danger signals: Chemotherapy enhancers?

2017

IF 9.614; International audience; Endogenous danger signals are molecules normally present in a given cell compartment that are rapidly released following cell stress and induce immune responses. We and others have shown that dying tumor cells treated with some chemotherapies are able to induce anticancer immune responses, which rely on their release of danger signals such as the nuclear protein HMGB1. DNA can also be released from chemotherapy-treated tumor cells, act as a danger signal, and boost anticancer immunity. While the immunostimulatory properties of DNA have been identified for decades, the recent discovery of a novel family of receptors, cytosolic DNA sensors, has provided a nov…

0301 basic medicineImmunologyCelleducationBiologyHMGB1CD8+ T cellschemotherapyCancer Vaccines03 medical and health sciences0302 clinical medicineImmune systemDrug TherapyNeoplasmsmedicineImmunology and AllergyCytotoxic T cellAnimalsHumanscancer[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMolecular Targeted TherapyNuclear proteinHMGB1 ProteinReceptorinnate immunityInnate immune systemDNAadaptive immunityAcquired immune systemCombined Modality TherapyImmunity Innate3. Good health030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinCancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunotherapy030215 immunologySignal TransductionSTINGImmunological Reviews
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NKG2D stimulation of CD8(+) T cells during priming promotes their capacity to produce cytokines in response to viral infection in mice

2017

NKG2D is an activating receptor that is expressed on most cytotoxic cells of the immune system, including NK cells, γδ and CD8+ T cells. It is still a matter of debate whether and how NKG2D mediates priming of CD8+ T cells in vivo, due to a lack of studies where NKG2D is eliminated exclusively in these cells. Here we studied the impact of NKG2D on effector CD8+ T-cell formation. NKG2D-deficiency that is restricted to murine CD8+ T cells did not impair antigen-specific T-cell expansion following mCMV and LCMV infection, but reduced their capacity to produce cytokines. Upon infection, conventional dendritic cells induce NKG2D ligands, which drive cytokine production on CD8+ T cells via the Da…

0301 basic medicineImmunologyCytokines ; Dap10 ; Effector CD8+ T cells ; LCMV ; NKG2D ; mCMVchemical and pharmacologic phenomenaBiologyCD8+ T cellsNKG2D03 medical and health sciencesInterleukin 21Immunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellZAP70BIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.hemic and immune systemsNKG2DNatural killer T cellmCMVbiological factors3. Good health030104 developmental biologyCostimulationPrimingImmunologyInterleukin 12CytokinesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.European journal of immunology
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Revisiting Type 2-high and Type 2-low airway inflammation in asthma: current knowledge and therapeutic implications

2017

Asthma is a complex respiratory disorder characterized by marked heterogeneity in individual patient disease triggers and response to therapy. Several asthma phenotypes have now been identified, each defined by a unique interaction between genetic and environmental factors, including inflammatory, clinical and trigger-related phenotypes. Endotypes further describe the functional or pathophysiologic mechanisms underlying the patient's disease. type 2-driven asthma is an emerging nomenclature for a common subtype of asthma and is characterized by the release of signature cytokines IL-4, IL-5 and IL-13 from cells of both the innate and adaptive immune systems. A number of well-recognized bioma…

0301 basic medicineImmunologyDiseasePeriostin03 medical and health sciencesTh2 Cells0302 clinical medicineImmune systemT-Lymphocyte SubsetsmedicineAnimalsHumansImmunology and AllergyAsthmaInflammationbusiness.industrymedicine.diseasePhenotypeAsthmaPathophysiologyrespiratory tract diseases030104 developmental biology030228 respiratory systemExhaled nitric oxideImmunologyCytokinesSputumInflammation Mediatorsmedicine.symptombusinessBiomarkersSignal TransductionClinical & Experimental Allergy
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Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

2014

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL…

0301 basic medicineImmunologyGraft vs Host DiseaseInflammationReceptor Interferon alpha-betaInterleukin 2203 medical and health sciencesMiceInterferonimmune system diseasesBone MarrowmedicineImmunology and AllergyCXCL10AnimalsTransplantation HomologousHumansSTAT1Intestine LargeIntestinal MucosaBone Marrow TransplantationMice KnockoutMice Inbred BALB CbiologyInterleukinsTh1 CellsTissue DonorsTransplantationMice Inbred C57BLChemokine CXCL10030104 developmental biologymedicine.anatomical_structuresurgical procedures operativeSTAT1 Transcription FactorGene Expression RegulationHematologic NeoplasmsImmunologyInterferon Type Ibiology.proteinSTAT proteinBone marrowmedicine.symptomWhole-Body Irradiationmedicine.drugSignal Transduction
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TLR4 participates in the transmission of ethanol-induced neuroinflammation via astrocyte-derived extracellular vesicles

2019

Background Current evidence indicates that extracellular vesicles (EVs) participate in intercellular signaling, and in the regulation and amplification of neuroinflammation. We have previously shown that ethanol activates glial cells through Toll-like receptor 4 (TLR4) by triggering neuroinflammation. Here, we evaluate if ethanol and the TLR4 response change the release and inflammatory content of astrocyte-derived EVs, and whether these vesicles are capable of communicating with neurons by spreading neuroinflammation. Methods Cortical neurons and astrocytes in culture were used. EVs were isolated from the extracellular medium of the primary culture of the WT and TLR4-KO astrocytes treated …

0301 basic medicineImmunologyInflammationlcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineWestern blotNeuroinflammationGlial cellsExtracellularmedicineAnimalsProtein Interaction MapsReceptorNeuroinflammationCells Culturedlcsh:Neurology. Diseases of the nervous systemInflammationMice KnockoutNeuronsmedicine.diagnostic_testEthanolChemistryGeneral NeuroscienceResearchExtracellular vesiclesCell biologyMice Inbred C57BLToll-Like Receptor 4030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTLR4medicine.symptom030217 neurology & neurosurgeryIntracellularAstrocyteJournal of Neuroinflammation
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Frontline Science: Mast cells regulate neutrophil homeostasis by influencing macrophage clearance activity

2019

Abstract The receptor tyrosine kinase cKit and its ligand stem cell factor are essential for mast cells (MC) development and survival. Strains with mutations affecting the Kit gene display a profound MC deficiency in all tissues and have been extensively used to investigate the role of MC in both physiologic and pathologic conditions. However, these mice present a variety of abnormalities in other immune cell populations that can affect the interpretation of MC-related responses. C57BL/6 KitW-sh are characterized by an aberrant extramedullary myelopoiesis and systemic neutrophilia. MC deficiency in KitW-sh mice can be selectively repaired by engraftment with in vitro-differentiated MC to va…

0301 basic medicineImmunologyKit (W-sh) mice; macrophages; mast cell; neutrophils; phagocytosisBone Marrow CellsCell CountStem cell factormacrophageReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineImmune systemneutrophilsGranulocyte Colony-Stimulating FactormedicineAnimalsHomeostasisImmunology and AllergyMacrophageMyeloid CellsMast CellsNeutrophil homeostasisCD11b AntigenNeutrophil clearancebiologyInterleukin-17neutrophilphagocytosisCell BiologyKit (W-sh) miceNeutrophiliaHematopoiesismacrophagesCell biologyMice Inbred C57BLProto-Oncogene Proteins c-kitPhenotype030104 developmental biologybiology.proteinCytokinesInflammation Mediatorsmedicine.symptommast cellEx vivoSignal Transduction030215 immunologyJournal of Leukocyte Biology
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Group 3 Innate Lymphoid Cells Program a Distinct Subset of IL-22BP-Producing Dendritic Cells Demarcating Solitary Intestinal Lymphoid Tissues.

2019

Solitary intestinal lymphoid tissues such as cryptopatches (CPs) and isolated lymphoid follicles (ILFs) constitute steady-state activation hubs containing group 3 innate lymphoid cells (ILC3) that continuously produce interleukin (IL)-22. The outer surface of CPs and ILFs is demarcated by a poorly characterized population of CD11c+ cells. Using genome-wide single-cell transcriptional profiling of intestinal mononuclear phagocytes and multidimensional flow cytometry, we found that CP- and ILF-associated CD11c+ cells were a transcriptionally distinct subset of intestinal cDCs, which we term CIA-DCs. CIA-DCs required programming by CP- and ILF-resident CCR6+ ILC3 via lymphotoxin-β receptor sig…

0301 basic medicineImmunologyPopulationCD11cGene ExpressionMice TransgenicC-C chemokine receptor type 6BiologyFlow cytometryImmunophenotyping03 medical and health sciencesMicePeyer's Patches0302 clinical medicineRNA Small CytoplasmicmedicineImmunology and AllergyAnimalsIntestinal Mucosaeducationeducation.field_of_studymedicine.diagnostic_testGene Expression ProfilingInnate lymphoid cellInterleukinDendritic CellsReceptors InterleukinLipid MetabolismImmunity InnateLymphocyte SubsetsCell biology030104 developmental biologyInfectious DiseasesLymphotoxinGene Expression Regulation030220 oncology & carcinogenesisHomeostasisBiomarkersSignal TransductionImmunity
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Antigen-dependent competition shapes the local repertoire of tissue-resident memory CD8+ T cells.

2016

Muschaweckh et al. show that antigen presentation in the skin regulates the generation of tissue-resident memory T (TRM) cells by orchestrating local competition of antiviral CD8+ T cells, revealing a mechanism to fine-tune the repertoire of regional pools of TRM cells.

0301 basic medicineImmunologyReceptors Antigen T-CellMice TransgenicVaccinia virusCell fate determinationBiologyCD8-Positive T-LymphocytesVirusArticle31203 medical and health sciencesMice0302 clinical medicineAntigen319VacciniaImmunology and AllergyCytotoxic T cellAnimalsAntigens ViralResearch ArticlesCell growthRepertoireT-cell receptorVirology030104 developmental biologyCD8030215 immunologySignal Transduction
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IL-17 polarization of MAIT cells is derived from the activation of two different pathways

2017

MAIT cells are expanded in salivary glands of patients with Sjogren's syndrome and are IL-17 polarized. IL-7 and IL-23 induce IL-17 production activating two different pathways: IL-7 stimulation induces in fact a significant STAT3 and HIF1alpha upregulation, conversely, IL-23 stimulation significantly induces RORc overexpression in MAIT cells of patients with Sjogren's syndrome.

0301 basic medicineImmunologyStimulationInterleukin-23Mucosal-Associated Invariant T CellsSalivary GlandsSTAT303 medical and health sciencesIL-17; IL-23; IL-7; MAIT cells; RORc; Sjogren's Syndrome; STAT3; Immunology and Allergy; Immunology0302 clinical medicinestomatognathic systemDownregulation and upregulationRAR-related orphan receptor gammaIL-23Interleukin 23HumansImmunology and AllergySTAT3MAIT cellIL-7biologyInterleukin-17MAIT CellsCell biologyRORcIL-17Settore MED/16 - Reumatologia030104 developmental biologySjogren's Syndromebiology.proteinInterleukin 17030215 immunology
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HSP110 sustains chronic NF-κB signaling in activated B cell diffuse large B cell lymphoma through MyD88 stabilization

2018

International audience; Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive lymphoproliferative disorder involving chronic NF-κB activation. Several mutations in the BCR and the MyD88 signaling pathway components, such as MyD88 L265P, are implicated in this aberrant activation. Among heat-shock proteins, HSP110 has recently been identified as a pro- survival and/or proliferation factor in many cancers but its role in ABC-DLBCL survival mechanisms remained to be established. We observed that shRNA-mediated HSP110 silencing decreased the survival of several ABC-DLBCL cell lines, decreased IgM-MyD88 co-localization and subsequent NF-κB signaling. Conversely, over-expres…

0301 basic medicineImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies03 medical and health sciencesimmune system diseaseshemic and lymphatic diseasesmedicineTumor Cells CulturedGene silencingHumansHSP110 Heat-Shock ProteinsB cellChemistryProtein StabilityWild typebreakpoint cluster regionNF-kappa BCell BiologyHematologymedicine.disease3. Good healthLymphoma030104 developmental biologymedicine.anatomical_structureCell cultureMyeloid Differentiation Factor 88Cancer researchLymphoma Large B-Cell DiffuseSignal transductionDiffuse large B-cell lymphomaSignal Transduction
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