Search results for "Lymphocyte"

showing 10 items of 2280 documents

Exogenous TNFR2 activation protects from acute GvHD via host T reg cell expansion

2015

Activation of TNFR2 with a novel agonist expands T reg cells in vivo and protects allo-HCT recipients from acute GvHD while sparing antilymphoma and antiinfectious properties of transplanted donor T cells.

0301 basic medicineInterleukin 2medicine.medical_treatmentImmunologyGraft vs Host DiseaseMice Inbred Strainschemical and pharmacologic phenomenaHematopoietic stem cell transplantationBiologyT-Lymphocytes RegulatoryArticleMice03 medical and health sciencesInterleukin 21immune system diseaseshemic and lymphatic diseasesmedicineAnimalsReceptors Tumor Necrosis Factor Type IIImmunology and AllergyCytotoxic T cellddc:610Research Articlesintegumentary systemMyeloid-Derived Suppressor CellsHematopoietic Stem Cell TransplantationFOXP3hemic and immune systemsmedicine.diseaseLeukemiaddc:57030104 developmental biologysurgical procedures operativeAcute DiseaseImmunologyMyeloid-derived Suppressor CellInterleukin-2FemaleTumor necrosis factor receptor 2medicine.drug
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ILC3 in Axial Spondyloarthritis: the Gut Angle

2019

Purpose of Review: A growing body of evidence supports the relevance of the interleukin-23/interleukin-17 (IL-23/IL-17) pathway for the pathogenesis of axial spondyloarthritis (axSpA) and its treatment. Recently, innate lymphoid cells (ILC), a heterogeneous family of immune effector cells, have been identified as a relevant contributor in tissue homeostasis, partially via IL-23/IL-17 axis. This review describes the biology and the origins of the group 3 ILCs (ILC3s) in humans, focusing on their role in the pathogenesis of axSpA. Recent Findings: Clinical trials showed the effectiveness of IL23/IL-17 axis inhibition in both spondyloarthritis (SpA) and Inflammatory Bowel Disease (IBD). Recent…

0301 basic medicineInterleukin-23Inflammatory bowel diseasePathogenesis03 medical and health sciences0302 clinical medicineRheumatologySpondyloarthritisSpondylarthritismedicineInterleukin 23HumansLymphocytesIL-23/IL-17 axiGut inflammationTissue homeostasisInflammation030203 arthritis & rheumatologyAnkylosing spondylitisInnate immune systembusiness.industryInterleukin-17Innate lymphoid cellLymphoid tissue inducer cellmedicine.diseaseImmunity InnateAnkylosing spondylitiIL-17030104 developmental biologyImmunologyInterleukin 17businessGroup 3 innate lymphoid cellCurrent Rheumatology Reports
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Dermal CD207-Negative Migratory Dendritic Cells Are Fully Competent to Prime Protective, Skin Homing Cytotoxic T-Lymphocyte Responses

2018

Dendritic cells (DCs) are important inducers and regulators of T-cell responses. They are able to activate and modulate the differentiation of CD4+ and CD8+ T cells. In the skin, there are at least five phenotypically distinct DC subpopulations that can be distinguished by differential expression of the cell surface markers CD207, CD103, and CD11b. Previous studies have suggested that dermal CD11b−CD207+ conventional type 1 DCs are indispensable for the priming of a skin homing cytotoxic T-lymphocyte response. However, conventional type 1 DCs are also the only skin DC subset capable of cross-presenting exogenous antigens on major histocompatibility complex class I. Thus, it remained unclear…

0301 basic medicineLangerhans cellEpitopes T-LymphocytePriming (immunology)Mice TransgenicVaccinia virusDermatologyCD8-Positive T-LymphocytesBiologyMajor histocompatibility complexBiochemistryMice03 medical and health sciencesCross-Priming0302 clinical medicineAntigenmedicineAnimalsHumansCytotoxic T cellMolecular BiologySkinintegumentary systemCluster of differentiationHistocompatibility Antigens Class ICell BiologyDendritic cellCell biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureLangerhans Cells030220 oncology & carcinogenesisSkin Diseases Viralbiology.proteinImmunologic MemoryCD8T-Lymphocytes CytotoxicJournal of Investigative Dermatology
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Selective AhR knockout in langerin-expressing cells abates Langerhans cells and polarizes Th2/Tr1 in epicutaneous protein sensitization

2020

The aryl hydrocarbon receptor (AhR) represents an environmental sensor regulating immune responses. In the skin, AhR is expressed in several cell types, including keratinocytes, epidermal Langerhans cells (LC), and dermal dendritic cells (DC). The mechanisms how AhR activates or inhibits cutaneous immune responses remain controversial, owing to differences in the cell-specific functions of AhR and the different activating ligands. Therefore, we sought to investigate the role of AhR in LC and langerin(+) and negative DC in the skin. To this aim, we generated Langerin-specific and CD11c-specific knockout ((−/−)) mice lacking AhR, respectively, in LC and Langerin(+) dermal DC and in all CD11c(…

0301 basic medicineLangerinOvalbuminMice TransgenicAdministration CutaneousImmunoglobulin ET-Lymphocytes RegulatoryGene Knockout TechniquesMice03 medical and health sciencesTh2 Cells0302 clinical medicineImmune systemBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsLectins C-TypeInterleukin 5SensitizationMultidisciplinaryintegumentary systembiologyChemistryImmunoglobulin EBiological Sciencesrespiratory systemAryl hydrocarbon receptorMolecular biologyOvalbuminMannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureReceptors Aryl HydrocarbonLangerhans CellsAntigens SurfaceInterleukin 13biology.proteinEpidermis030215 immunologyProceedings 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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Microenvironmental Th9 and Th17 lymphocytes induce metastatic spreading in lung cancer.

2020

Immune microenvironment plays a critical role in lung cancer control versus progression and metastasis. In this investigation, we explored the effect of tumor-infiltrating lymphocyte subpopulations on lung cancer biology by studying in vitro cocultures, in vivo mouse models, and human lung cancer tissue. Lymphocyte conditioned media (CM) induced epithelial-mesenchymal transition (EMT) and migration in both primary human lung cancer cells and cell lines. Correspondingly, major accumulation of Th9 and Th17 cells was detected in human lung cancer tissue and correlated with poor survival. Coculturing lung cancer cells with Th9/Th17 cells or exposing them to the respective CM induced EMT in canc…

0301 basic medicineLymphocyteT cellsInflammationMetastasis03 medical and health sciences0302 clinical medicinemedicineLung cancerCancerInflammationbiologybusiness.industryCancerGeneral Medicinemedicine.disease030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchmedicine.symptomAntibodybusiness
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Studying Tumor-ReacTive T Cells: A Personalized Organoid Model.

2018

Cancer immunotherapies have shown substantial clinical activity for a subset of patients with epithelial cancers. Still, technological platforms to study cancer – T cell interactions for individual patients, and understand determinants of responsiveness, are presently lacking. Here, we establish and validate a platform to induce and analyze tumor-specific T cell responses for epithelial cancers in a personalized manner. We demonstrate that co-cultures of autologous tumor organoids and peripheral blood lymphocytes can be used to enrich for tumor-reactive T cells from peripheral blood of patients with mismatch repair deficient colorectal cancer and non-small cell lung cancer. Furthermore, we …

0301 basic medicineLymphocyteT-LymphocytesTranslation (biology)Cell BiologyBiologyCoculture TechniquesArticleOrganoids03 medical and health sciences030104 developmental biologymedicine.anatomical_structureNeoplasmsGeneticsmedicineCancer researchOrganoidMolecular MedicineCoculture TechniqueHumansValue (mathematics)Cell stem cell
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Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics

2016

NKX2 homeobox family proteins have a role in cancer development. Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malignancies. While Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of tumours, faithfully recapitulating the principal clinical and biological features of human marginal-zone lymphomas. NKX2-3 induces B-cell receptor signalling by phosphorylating Lyn/Syk kinases, which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) a…

0301 basic medicineLymphoid TissueScienceB-cell receptorReceptors Antigen B-CellGeneral Physics and AstronomySykKaplan-Meier EstimateBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyNKX2-303 medical and health sciencesChemokine receptorstomatognathic systemLYNhemic and lymphatic diseasesmedicineAnimalsHumansSyk KinaseLymphocytesPhosphorylationB cellHomeodomain ProteinsMice KnockoutCàncer -- Aspectes molecularsMultidisciplinaryCell adhesion moleculeKinaseGene Expression ProfilingQLymphoma B-Cell Marginal ZoneGeneral Chemistryrespiratory system3. Good healthMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureembryonic structurescardiovascular systemCancer researchCell Adhesion MoleculesProteïnesSignal TransductionTranscription FactorsNature Communications
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Targeting prohibitins at the cell surface prevents Th17-mediated autoimmunity.

2018

T helper (Th)17 cells represent a unique subset of CD4(+) T cells and are vital for clearance of extracellular pathogens including bacteria and fungi. However, Th17 cells are also involved in orchestrating autoimmunity. By employing quantitative surface proteomics, we found that the evolutionarily conserved prohibitins (PHB1/2) are highly expressed on the surface of both murine and human Th17 cells. Increased expression of PHBs at the cell surface contributed to enhanced CRAF/MAPK activation in Th17 cells. Targeting surface‐expressed PHBs on Th17 cells with ligands such as Vi polysaccharide (Typhim vaccine) inhibited CRAF‐MAPK pathway, reduced interleukin (IL)‐17 expression and ameliorated …

0301 basic medicineMAPK/ERK pathwayMultiple SclerosisT cellCellPopulationAutoimmunityBiologymedicine.disease_causeT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyAutoimmunity03 medical and health sciencesMiceProhibitinsRickettsial VaccinesmedicineAnimalsHumanseducationExtracellular Signal-Regulated MAP KinasesMolecular Biologyeducation.field_of_studyGeneral Immunology and MicrobiologyGeneral NeuroscienceInterleukinFOXP3Forkhead Transcription FactorsArticlesCell biologyRepressor Proteins030104 developmental biologymedicine.anatomical_structureTh17 CellsSignal transductionHeLa CellsSignal TransductionThe EMBO journal
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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