Search results for "Immunity"

showing 10 items of 1537 documents

The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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CD36 as a lipid sensor

2011

International audience; CD36 is a multifunctional protein homologous to the class B scavenger receptor SR-B1 mainly found in tissues with a sustained lipid metabolism and in several hematopoieic cells. CD36 is thought to be involved in various physiological and pathological processes like angiogenesis, thrombosis, atherogenesis, Alzheimer's disease or malaria. An additive emerging function for CD36 is a role as a lipid sensor. Location of CD36 and orthologue molecules in plasma membrane of cells in contact with the external environment (e.g. gustatory, intestinal or olfactory epithelia) allows the binding of exogenous-derived ligands including dietary lipids, diglycerides from bacterial wal…

CD36 AntigensAngiogenesisFat preference[SDV]Life Sciences [q-bio]CD36Peroxisome proliferator-activated receptorExperimental and Cognitive PsychologyBiology03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineLipid-binding proteinparasitic diseasesAnimalsScavenger receptor030304 developmental biologyG protein-coupled receptorNeuronschemistry.chemical_classificationBehavior0303 health sciencesInnate immune systemCell MembraneBrainLipid metabolismLipid MetabolismLipidsImmunity InnateLipid receptors3. Good healthBiochemistrychemistrybiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryFunction (biology)Physiology & Behavior
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Innate Effector-Memory T-Cell Activation Regulates Post-Thrombotic Vein Wall Inflammation and Thrombus Resolution

2016

Rationale: Immune cells play an important role during the generation and resolution of thrombosis. T cells are powerful regulators of immune and nonimmune cell function, however, their role in sterile inflammation in venous thrombosis has not been systematically examined. Objective: This study investigated the recruitment, activation, and inflammatory activity of T cells in deep vein thrombosis and its consequences for venous thrombus resolution. Methods and Results: CD4 + and CD8 + T cells infiltrate the thrombus and vein wall rapidly on deep vein thrombosis induction and remain in the tissue throughout the thrombus resolution. In the vein wall, recruited T cells largely consist of effect…

CD4-Positive T-Lymphocytes0301 basic medicineChemokineMice 129 StrainPhysiologyMice TransgenicInflammationCD8-Positive T-Lymphocytes030204 cardiovascular system & hematologyVaricose VeinsMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansThrombusVeinInflammationVenous ThrombosisbiologyEffector Memory T-CellThrombosismedicine.diseaseThrombosisImmunity InnateCell biologyMice Inbred C57BLVenous thrombosis030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinmedicine.symptomCardiology and Cardiovascular MedicineCirculation Research
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A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
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Opposing functions of thymic stromal lymphopoietin–responsive basophils and dendritic cells in a mouse model of atopic dermatitis

2015

CD4-Positive T-Lymphocytes0301 basic medicineThymic stromal lymphopoietinImmunologyInflammationAdaptive ImmunityImmunoglobulin EDermatitis AtopicMice03 medical and health sciences0302 clinical medicineThymic Stromal LymphopoietinAnimalsImmunology and AllergyMedicineInterleukin 4Inflammationbiologybusiness.industryDendritic CellsAtopic dermatitisImmunoglobulin EAcquired immune systemmedicine.diseaseBasophilsMice Inbred C57BLDisease Models Animal030104 developmental biologyImmunologybiology.proteinCytokinesInterleukin-4medicine.symptombusiness030215 immunologyJournal of Allergy and Clinical Immunology
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B cells participate in thymic negative selection of murine auto-reactive CD4+ T cells.

2010

It is well documented that thymic epithelial cells participate in the process of negative selection in the thymus. In recent years it was reported that also dendritic cells enter the thymus and contribute to this process, thus allowing for the depletion of thymocytes that are specific to peripherally expressed self-antigens. Here we report that also B cells may take part in the elimination of auto-reactive thymocytes. Using a unique mouse model we show that B cells induce negative selection of self-reactive thymocytes in a process that leads to the deletion of these cells whereas regulatory T cells are spared. These findings have direct implication in autoimmunity, as expression of a myelin…

CD4-Positive T-LymphocytesB CellsImmune CellsImmunologyCD1Antigen-Presenting Cellslcsh:MedicineAutoimmunityMice TransgenicThymus GlandBiologyMiceNegative selectionAntigenImmune ToleranceAnimalsIL-2 receptorAntigen-presenting celllcsh:ScienceBiologyClonal AnergyB-LymphocytesMultidisciplinaryCD40Clonal anergyT Cellslcsh:RImmunityCell biologyImmunologyInterleukin 12biology.proteinlcsh:QResearch ArticlePLoS ONE
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Assessment of local cellular immunity in lung cancer by bronchoalveolar lavage.

1990

Small cell lung cancer (SCLC) is the most malignant of the pulmonary neoplasms and is associated with a poor local cellular immune response. 16 patients with non small cell lung cancer (NSCLC) and 11 patients with SCLC underwent bronchoalveolar lavage (BAL) in the lung which harbored the tumor in order to investigate the lymphocyte surface antigens utilizing the immunoperoxidase technique. Analysis of blood lymphocytes was performed in parallel. 8 patients with previous sarcoidosis in complete remission who underwent BAL and 10 normal blood donors served as controls. Among blood lymphocytes the CD3+, CD4+ and CD16+ cell populations were elevated significantly and the T4/T8 ratio was elevate…

CD4-Positive T-LymphocytesCellular immunityPathologymedicine.medical_specialtyLung NeoplasmsLymphocyteT-LymphocytesAdenocarcinomaLeukocyte CountImmune systemAntigens CDCarcinoma Non-Small-Cell LungDrug DiscoveryImmune ToleranceMedicineHumansCarcinoma Small CellLung cancerGenetics (clinical)Lungmedicine.diagnostic_testImmunoperoxidasebusiness.industryReceptors Interleukin-2General Medicinerespiratory systemmedicine.diseaserespiratory tract diseasesBronchoalveolar lavagemedicine.anatomical_structureImmunologyCarcinoma Squamous CellMolecular MedicineSarcoidosisbusinessBronchoalveolar Lavage FluidKlinische Wochenschrift
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Timing of activation of CD4+ memory cells as a possible marker to establish the efficacy of vaccines against contagious agalactia in sheep

2013

Mycoplasma agalactiae is a major pathogen of sheep and goats in many areas of the world and particularly in Mediterranean countries. It causes contagious agalactia, an infectious disease primarily affecting mammary glands. Many vaccines against the pathogen are currently under development. The aim of the study was to investigate the involvement of T cell-mediated immunity during vaccination and challenge experiments against Mycoplasma agalactiae. A comparison of the antigen-specific expansion of interferon gamma positive T cell memory and naïve subsets was performed between vaccinated and non-vaccinated sheep to identify cellular subsets whose activation was different between protected and …

CD4-Positive T-LymphocytesCellular immunityTime FactorsT cellMycoplasma agalactiaeImmunologyved/biology.organism_classification_rank.speciesSheep DiseasesCD8-Positive T-LymphocytesBiologyLymphocyte ActivationMycoplasma agalactiaeInterferon-gammaT-Lymphocyte SubsetsImmunitymedicineAnimalsMycoplasma InfectionsInterferon gammaMycoplasma agalactiae Cellular immunity IFN-g + cellsPathogenSheep DomesticSheepGeneral Veterinaryved/biologyVaccine efficacyAntibodies BacterialVirologyVaccinationTreatment Outcomemedicine.anatomical_structureImmunoglobulin GBacterial VaccinesImmunologyFemaleImmunologic Memorymedicine.drugVeterinary Immunology and Immunopathology
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Cross-recognition of a myelin peptide by CD8+ T cells in the CNS is not sufficient to promote neuronal damage.

2015

Multiple sclerosis (MS) is an inflammatory disease of the CNS thought to be driven by CNS-specific T lymphocytes. Although CD8+T cells are frequently found in multiple sclerosis lesions, their distinct role remains controversial because direct signs of cytotoxicity have not been confirmedin vivo. In the present work, we determined that murine ovalbumin-transgenic (OT-1) CD8+T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40–54 (MOG40–54) bothin vitroandin vivo. The aim of this study was to investigate whether such cross-recognizing CD8+T cells are capable of inducing CNS damagein vivo. Using intravital two-photon microscopy in the mouse model of multiple sclerosis, …

CD4-Positive T-LymphocytesCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisAutoimmunityMice TransgenicCD8-Positive T-Lymphocytesmedicine.disease_causeMyelin oligodendrocyte glycoproteinMyelinMiceIn vivomedicineCytotoxic T cellAnimalsCells CulturedCell ProliferationbiologyCell DeathGeneral NeuroscienceMultiple sclerosisArticlesmedicine.diseaseMolecular mimicrymedicine.anatomical_structureImmunologyNerve Degenerationbiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinCD8Intravital microscopyThe Journal of neuroscience : the official journal of the Society for Neuroscience
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The role of Th1/Th2 polarization in mucosal immunity

2002

Mucosal immunity relies on the delicate balance between antigen responsiveness and tolerance. The polarization of T helper cells plays a key role in maintaining or disrupting this equilibrium.

CD4-Positive T-LymphocytesChemistryModels ImmunologicalCell PolarityGeneral MedicineTh1 CellsInflammatory Bowel DiseasesAsthmaGeneral Biochemistry Genetics and Molecular BiologyTh2 polarizationTh2 CellsAntigenImmunityImmunologyAnimalsHumansImmunity MucosalMucosal immunityNature Medicine
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