Search results for "Langerhan"

showing 10 items of 138 documents

Production of Extracellular Adenosine by CD73+ Dendritic Cells Is Crucial for Induction of Tolerance in Contact Hypersensitivity Reactions

2019

Dendritic cells (DCs) express the ecto-5′-nucleotidase CD73 that generates immunosuppressive adenosine (Ado) by dephosphorylation of extracellular Ado monophosphate and diphosphate. To investigate whether CD73-derived Ado has immune-suppressive activity, 2,4-dinitrothiocyanobenzene (DNTB) was applied to skin of wild-type (WT) or CD73-deficient (CD73–/–) mice, followed by sensitization and challenge with 2,4-dinitrofluorobenzene. In this model, we show the induction of tolerance by DNTB against 2,4-dinitrofluorobenzene only in WT but not in CD73–/– mice. Analysis of skin DCs showed increased expression of CD73 after application of DNTB in WT mice. That was accompanied by elevated concentrati…

0301 basic medicineAdenosine monophosphateLangerhans cellRegulatory T cellTransgeneCell BiologyDermatologyDendritic cellBiochemistryAdenosineCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinemedicine.anatomical_structurechemistry030220 oncology & carcinogenesisExtracellularmedicineCyclic adenosine monophosphateMolecular Biologymedicine.drugJournal of Investigative Dermatology
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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E-Cadherin is Dispensable to Maintain Langerhans Cells in the Epidermis.

2019

The cell adhesion molecule E-cadherin is a major component of adherens junctions and marks Langerhans cells (LC), the only dendritic cell (DC) population of the epidermis. LC form a dense network and attach themselves to the surrounding keratinocytes via homophilic E-cadherin binding. LC activation, mobilization, and migration require a reduction in LC E-cadherin expression. To determine whether E-cadherin plays a role in regulating LC homeostasis and function, we generated CD11c-specific E-cadherin knockout mice (CD11c-Ecaddel). In the absence of E-cadherin−mediated cell adhesion, LC numbers remained stable and similar as in control mice, even in aged animals. Intriguingly, E-cadherin−defi…

0301 basic medicineCellular differentiationPopulationDermatologyDermatitis ContactBiochemistryAdherens junction03 medical and health sciencesMice0302 clinical medicineCell MovementAnimalsHomeostasisHumansPsoriasisCell adhesioneducationMolecular BiologyCell ShapeCells CulturedMice Knockouteducation.field_of_studyImiquimodEpidermis (botany)CadherinCell adhesion moleculeChemistryCell DifferentiationCell BiologyDendritic cellCadherinsCell biologyCD11c AntigenDisease Models Animal030104 developmental biology030220 oncology & carcinogenesisLangerhans CellsEpidermisThe Journal of investigative dermatology
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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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Langerhans Cells Suppress CD8+ T Cells In Situ during Mucocutaneous Acute Graft-Versus-Host Disease

2021

Acute graft-versus-host disease (aGVHD) induced by allogenic hematopoietic stem cell transplantation is an immunological disorder in which donor lymphocytes attack recipient organs. It has been proven that recipient nonhematopoietic tissue cells, such as keratinocytes, are sufficient as immunological targets for allogenic donor T cells, whereas Langerhans cells (LCs) are potent professional hematopoietic antigen-presenting cells existing in the target epidermis and eliminated during the early phase of mucocutaneous aGVHD. Moreover, LCs have been reported to negatively regulate various types of immune responses. Here, we present data showing that initial depletion of recipient LCs exacerbate…

0301 basic medicineLangerhans cellintegumentary systemRegulatory T cellMucocutaneous zoneCell BiologyDermatologyDendritic cellBiologyBiochemistry03 medical and health sciencesHaematopoiesis030104 developmental biology0302 clinical medicinemedicine.anatomical_structureImmune system030220 oncology & carcinogenesisCancer researchmedicineCytotoxic T cellBone marrowMolecular BiologyJournal 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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3d collagen hydrogel promotes in vitro langerhans islets vascularization through ad-mvfs angiogenic activity

2021

Adipose derived microvascular fragments (ad-MVFs) consist of effective vascularization units able to reassemble into efficient microvascular networks. Because of their content in stem cells and related angiogenic activity, ad-MVFs represent an interesting tool for applications in regenerative medicine. Here we show that gentle dissociation of rat adipose tissue provides a mixture of ad-MVFs with a length distribution ranging from 33–955 μm that are able to maintain their original morphology. The isolated units of ad-MVFs that resulted were able to activate transcriptional switching toward angiogenesis, forming tubes, branches, and entire capillary networks when cultured in 3D collagen type-…

0301 basic medicineMMP2QH301-705.5Angiogenesis0206 medical engineeringMedicine (miscellaneous)Adipose tissue3D coculture02 engineering and technologyRegenerative medicineGeneral Biochemistry Genetics and Molecular BiologyArticleExtracellular matrix03 medical and health sciencesmedicineBiology (General)Islet of LangerhansTransplantationChemistry020601 biomedical engineeringCell biologyTransplantationMicrovascular fragments030104 developmental biologymedicine.anatomical_structureBasal laminaAngiogenesisStem cell3D coculture; Angiogenesis; Islet of Langerhans; Microvascular fragments; Transplantation
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miRNA92a targets KLF2 and the phosphatase PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity.

2016

Aberrant immune activation mediated by T effector cell populations is pivotal in the onset of autoimmunity in type 1 diabetes (T1D). T follicular helper (TFH) cells are essential in the induction of high-affinity antibodies, and their precursor memory compartment circulates in the blood. The role of TFH precursors in the onset of islet autoimmunity and signaling pathways regulating their differentiation is incompletely understood. Here, we provide direct evidence that during onset of islet autoimmunity, the insulin-specific target T-cell population is enriched with a C-X-C chemokine receptor type 5 (CXCR5)(+)CD4(+) TFH precursor phenotype. During onset of islet autoimmunity, the frequency o…

0301 basic medicineMaleReceptors CXCR5endocrine systemAdolescentPopulationPrimary Cell CultureKruppel-Like Transcription FactorsAutoimmunityMice TransgenicNodBiologymedicine.disease_causeCXCR5Autoimmunity03 medical and health sciencesIslets of LangerhansMicePhosphatidylinositol 3-Kinases0302 clinical medicineMice Inbred NODmedicineAnimalsHumansIL-2 receptorKlf2 ; Pten-pi3k Signaling ; T Follicular Helper Cells ; Mirna92a ; Type 1 DiabeteseducationChildPI3K/AKT/mTOR pathwayNOD miceAutoantibodiesgeographyeducation.field_of_studyMultidisciplinarygeography.geographical_feature_categoryForkhead Box Protein O1PTEN PhosphohydrolaseAntagomirsT-Lymphocytes Helper-InducerIsletMicroRNAs030104 developmental biologyDiabetes Mellitus Type 1Gene Expression RegulationImmunologyCancer researchFemale030215 immunologySignal Transduction
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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In cutaneous leishmaniasis, induction of retinoic acid in skin-derived Langerhans cells is not sufficient for induction of parasite persistence-media…

2017

0301 basic medicineReceptors CCR7Retinoic acidLeishmaniasis CutaneousTretinoinCell CommunicationDermatologyBiologyT-Lymphocytes RegulatoryBiochemistryHost-Parasite InteractionsPersistence (computer science)Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCutaneous leishmaniasismedicineAnimalsHumansParasite hostingMolecular BiologyLeishmania majorSkinMice Knockoutmedicine.diseaseDisease Models Animal030104 developmental biologychemistryLangerhans CellsImmunologyLymph Nodes030215 immunologyJournal of Dermatological Science
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