Search results for "spleen"

showing 10 items of 308 documents

STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity

2020

Natural killer (NK) cells are important components of the innate immune defense against infections and cancers. Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that is essential for NK cell maturation and NK cell-dependent tumor surveillance. Two alternatively spliced isoforms of STAT1 exist: a full-length STAT1α and a C-terminally truncated STAT1β isoform. Aberrant splicing is frequently observed in cancer cells and several anti-cancer drugs interfere with the cellular splicing machinery. To investigate whether NK cell-mediated tumor surveillance is affected by a switch in STAT1 splicing, we made use of knock-in mice expressing either only the STAT1α (S…

0301 basic medicineCytotoxicity ImmunologicLymphomaNK cellsCell MaturationMice0302 clinical medicineInterferonImmunology and AllergyProtein IsoformsSTAT1Immunologic SurveillanceOriginal ResearchBone Marrow TransplantationReceptors InterferonInterleukin-15Mice KnockoutLymphopoiesisinterferonInterferon-Stimulated Gene Factor 3Cell biologySpecific Pathogen-Free OrganismsKiller Cells NaturalSTAT1 Transcription FactorOrgan SpecificityMHC class ISignal transductionsignal transductionmedicine.druglcsh:Immunologic diseases. AllergyLymphoid TissueImmunologyBiologyLymphocyte Depletion03 medical and health sciencesInterleukin-15 Receptor alpha SubunitCell Line TumormedicineAnimalsTranscription factorInnate immune systemisoformsMice Inbred C57BL030104 developmental biologyCancer cellSTAT proteinbiology.proteinlcsh:RC581-607IL-15RαSpleen030215 immunologyFrontiers in Immunology
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TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

2017

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8(+)CD103(+) DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune ence…

0301 basic medicineEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentCellular differentiationAutoimmunitychemical and pharmacologic phenomenaCD8-Positive T-LymphocytesBiologyT-Lymphocytes RegulatorySmad7 ProteinImmune toleranceMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmune TolerancemedicineAnimalsIndoleamine-Pyrrole 23-DioxygenaseMultidisciplinaryintegumentary systemExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsDendritic CellsDendritic cellTransforming growth factor betamedicine.diseaseCell biologyMice Inbred C57BLTolerance inductionBasic-Leucine Zipper Transcription Factors030104 developmental biologyCytokinePNAS PlusInterferon Regulatory FactorsImmunologybiology.proteinCytokinesSpleenCD8Signal Transduction030215 immunology
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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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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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EBI2 in splenic and local immune responses and in autoimmunity

2017

Abstract The seven transmembrane G protein-coupled receptor EBV-induced gene 2 (EBI2), also known as GPR183, is expressed in particular in immune cells. Activated by its endogenous ligands, which are a group of oxysterols, it functions as a chemo-attractant receptor, mediating cell migration. In coordination with other receptors, EBI2 plays important roles in controlling the migration of immune cells during the course of a T-dependent Ab response in the spleen. In recent years, it has become clear that EBI2 also has other roles to play in the immune system. Thus, EBI2 seems to be involved in innate immune responses, such as those mediated by TLR signaling, and it has been implicated in regi…

0301 basic medicineImmunologyAutoimmunitySpleenBiologymedicine.disease_causeReceptors G-Protein-CoupledAutoimmunity03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansImmunology and AllergyReceptorG protein-coupled receptorInnate immune systemGPR183Cell migrationCell Biologybiochemical phenomena metabolism and nutritionImmunity Innate030104 developmental biologymedicine.anatomical_structureImmunologybacteriaSpleen030217 neurology & neurosurgeryJournal of Leukocyte Biology
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Feedback Regulation of Syk by Protein Kinase C in Human Platelets

2019

The spleen tyrosine kinase (Syk) is essential for immunoreceptor tyrosine-based activation motif (ITAM)-dependent platelet activation, and it is stimulated by Src-family kinase (SFK)-/Syk-mediated phosphorylation of Y352 (interdomain-B) and Y525/526 (kinase domain). Additional sites for Syk phosphorylation and protein interactions are known but remain elusive. Since Syk S297 phosphorylation (interdomain-B) was detected in platelets, we hypothesized that this phosphorylation site regulates Syk activity via protein kinase C (PKC)-and cyclic adenosine monophosphate (cAMP)-dependent pathways. ADP, the GPVI-agonist convulxin, and the GPIb&alpha

0301 basic medicineIndolesPlatelet AggregationSyk030204 cardiovascular system & hematologyenvironment and public healthMaleimideslcsh:Chemistrychemistry.chemical_compound0302 clinical medicinePhosphorylationlcsh:QH301-705.5SpectroscopyFeedback PhysiologicalKinaseConvulxinhemic and immune systemsGeneral MedicineComputer Science ApplicationsCell biologyAdenosine DiphosphateplateletsPhosphorylationbiological phenomena cell phenomena and immunityBlood Plateletschemical and pharmacologic phenomenaViper Venomsspleen tyrosine kinase (Syk)CatalysisArticleInorganic Chemistryglycoprotein VIglycoprotein Ibα03 medical and health sciencesCrotalid VenomsHumansSyk KinaseCyclic adenosine monophosphateLectins C-TypePlatelet activationPhysical and Theoretical ChemistryMolecular BiologyProtein kinase CPhospholipase C gammaOrganic Chemistryenzymes and coenzymes (carbohydrates)030104 developmental biologyProtein kinase domainchemistrylcsh:Biology (General)lcsh:QD1-999Calciumcyclic adenosine monophosphate (cAMP)protein kinase CInternational Journal of Molecular Sciences
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Subcutaneous injection of exosomes reduces symptom severity and mortality induced by Echinostoma caproni infection in BALB/c mice.

2016

Recent studies have shown the importance of exosomes in the host-parasite relationship. These vesicles are an important part of the excretory/secretory pathway for proteins with the potential to alter immune responses. Therefore, in the present study, we examined the immunomodulatory role of exosomes in BALB/c mice using Echinostoma caproni as an experimental model of intestinal helminth infection. For this purpose, BALB/c mice were injected twice s.c. with purified exosomes of E. caproni, followed by experimental infection. We report a delay in the development of the parasite in mice immunised with exosomes, a concomitant reduced symptom severity and increased survival upon infection. Immu…

0301 basic medicineInjections Subcutaneous030231 tropical medicineAntibodies HelminthSpleenExosomesExosomeBALB/cHost-Parasite InteractionsImmunomodulation03 medical and health sciencesSubcutaneous injectionInterferon-gammaMiceRandom Allocation0302 clinical medicineImmune systemAntigenTransforming Growth Factor betaEchinostomamedicineAnimalsIntestinal Diseases ParasiticEchinostomiasisMice Inbred BALB Cbiologybiology.organism_classificationMicrovesiclesImmunoglobulin AInterleukin-10Disease Models Animal030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureImmunoglobulin MAntigens HelminthImmunoglobulin GImmunologybiology.proteinParasitologyFemaleInterleukin-4AntibodySpleenInternational journal for parasitology
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Host-based lipid inflammation drives pathogenesis in Francisella infection

2017

Mass spectrometry imaging (MSI) was used to elucidate host lipids involved in the inflammatory signaling pathway generated at the host-pathogen interface during a septic bacterial infection. Using Francisella novicida as a model organism, a bacterial lipid virulence factor (endotoxin) was imaged and identified along with host phospholipids involved in the splenic response in murine tissues. Here, we demonstrate detection and distribution of endotoxin in a lethal murine F. novicida infection model, in addition to determining the temporally and spatially resolved innate lipid inflammatory response in both 2D and 3D renderings using MSI. Further, we show that the cyclooxygenase-2-dependent lip…

0301 basic medicineLipopolysaccharideDIVERSITYGene ExpressionLIPOPOLYSACCHARIDEhost-pathogen interactionmedicine.disease_cause01 natural sciencesMass SpectrometryVirulence factorMicechemistry.chemical_compoundlipid inflammationcyclooxygenase pathwayHETEROGENEITYFrancisellaPhospholipidsMice KnockoutMultidisciplinarybiologyTULAREMIABiological SciencesMolecular ImagingHost-Pathogen InteractionsFrancisellalipids (amino acids peptides and proteins)FemaleSignal TransductionLPSHost–pathogen interactionmicrobial pathogenesismass spectrometry imagingDinoprostoneMicrobiologyCyclooxygenase pathwayProinflammatory cytokine03 medical and health sciencesImmune systemIMAGING MASS-SPECTROMETRYmedicineAnimalsBIOSYNTHESISFrancisella novicidaInflammationMacrophages010401 analytical chemistrybacterial infections and mycosesbiology.organism_classificationSurvival AnalysisImmunity Innate0104 chemical sciencesEndotoxinsMice Inbred C57BL030104 developmental biologychemistryCyclooxygenase 2EicosanoidsGram-Negative Bacterial InfectionsSpleenProceedings of the National Academy of Sciences
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Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization

2016

International audience; Objective: Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a pro…

0301 basic medicineLymphocyteIpid Transfer ProteinAdaptive ImmunityCardiovascular-DiseaseT-Lymphocytes RegulatoryLipoprotein MetabolismLeukocyte CountPhospholipid transfer proteinPolarizationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyHypersensitivity DelayedPhospholipid Transfer ProteinsCell PolarityCell DifferentiationT-Lymphocytes Helper-InducerT helper cellFlow CytometryAcquired immune systemCell biologyInfectious Diseasesmedicine.anatomical_structureEndothelial-CellsCytokines[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphocytemedicine.symptomResearch ArticleDensity-Lipoprotein[SDV.IMM] Life Sciences [q-bio]/ImmunologyHuman Atherosclerotic PlaquesT cellCirculating Interleukin-18ImmunologyT CellAntigen-Presenting CellsInflammationAcute Myocardial-InfarctionGATA3 Transcription FactorBiology03 medical and health sciencesImmune systemmedicineAnimalsAntigen-presenting cellDeficient MiceAlpha-TocopherolMice Inbred C57BL030104 developmental biologyImmunologyVitamin-ET-Box Domain ProteinsBiomarkersSpleen
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Impact of fascioliasis reinfection on Fasciola hepatica egg shedding: relationship with the immune-regulatory response.

2019

Abstract Fascioliasis is a disease caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm. Control strategies in humans require the use of egg count techniques to calculate the appropriate treatment dose for colic risk prevention. The present study investigates how fascioliasis reinfection affects liver fluke egg shedding and its relationship with the immune-regulatory response. The experimental design reproduced the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 4 weeks (R4), 8 weeks (R8), 12 weeks (R12), and negative control …

0301 basic medicineMaleFascioliasisVeterinary (miscellaneous)030231 tropical medicinePhysiologySpleenBiology03 medical and health sciences0302 clinical medicineImmune systemRecurrenceparasitic diseasesmedicineFasciola hepaticaAnimalsLongitudinal StudiesRats WistarParasite Egg CountEggs per gramFecesFOXP3030108 mycology & parasitologyLiver flukeFasciola hepaticabiology.organism_classificationInterleukin-10RatsInterleukin 10Infectious Diseasesmedicine.anatomical_structureCross-Sectional StudiesInsect ScienceImmunoglobulin GParasitologyActa tropica
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