Search results for " immune tolerance"

showing 8 items of 8 documents

Decellularized tracheal prelamination implant: A proposed bilateral double organ technique

2021

Introduction In tracheal replacement transplantation, prelamination is a critical stage. Nowadays, the most widely used prelamination technique is the prethoracic fascia flap with lateral thoracic artery. We propose a flap based on the internal thoracic artery, which allows a relatively non-aggressive double organ implant, and we have tested its efficacy in decellularized tracheas. Material and methods Tracheas of albino New Zealand rabbits were decellularized following a protocol that uses detergents and cryogenization, sterilized with 1kGy gamma radiation and tutorized with a stent. Bilateral pedicled flaps made of pectoral fascia and a muscular component were harvested through a longitud…

Malemedicine.medical_specialtyBiomedical EngineeringMedicine (miscellaneous)BioengineeringInternal thoracic arteryBiomaterialsmedicine.arterymedicineAnimalsTransplantation HomologousBioprosthesisDecellularizationCell-Free SystemTissue EngineeringLateral thoracic arterybusiness.industryGeneral MedicineFasciaPedicled FlapSurgeryTracheaTransplantationairway animal immune tolerance models tissue engineering trachea transplantsmedicine.anatomical_structureRabbitsImplantbusinessPectoral fasciaArtificial Organs
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Energetic reserves, leptin and testosterone: a refinement of the immunocompetence handicap hypothesis.

2007

Electronic supplementary material is available at http://dx.doi.org/10.1098/rsbl.2007.0020 or via http://www.journals.royalsoc.ac.uk.

0106 biological sciencesLeptinMalemedicine.medical_treatmentMESH : Analysis of Variance01 natural sciencesImmunocompetence handicap hypothesis[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]immunocompetence handicap hypothesis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsTestosteroneMESH : FinchesTestosterone0303 health sciencesSex CharacteristicsLeptinMESH : Immune ToleranceImmunosuppressionAgricultural and Biological Sciences (miscellaneous)Lipids3. Good health[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]MESH : Leptin[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH: FinchesImmunocompetenceGeneral Agricultural and Biological SciencesSex characteristicsMESH: Sex CharacteristicsResearch Articlemedicine.medical_specialtyMESH: Immune ToleranceMESH : MaleMESH: TestosteroneBiology010603 evolutionary biology03 medical and health sciencesImmune systemInternal medicineMESH: Analysis of VariancemedicineImmune ToleranceAnimals[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]030304 developmental biologyAnalysis of VarianceMESH : Sex CharacteristicsMESH : TestosteroneMESH : LipidsMESH: Leptinbiology.organism_classificationMESH: LipidsMESH: MaleEndocrinologyMESH : AnimalsFinchesTaeniopygiaHormoneBiology letters
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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Differential impact of high and low penetrance TNFRSF1A gene mutations on conventional and regulatory CD4+ T cell functions in TNFR1-associated perio…

2015

Abstract TNFR-associated periodic syndrome is an autoinflammatory disorder caused by autosomal-dominant mutations in TNFRSF1A, the gene encoding for TNFR superfamily 1A. The lack of knowledge in the field of TNFR-associated periodic syndrome biology is clear, particularly in the context of control of immune self-tolerance. We investigated how TNF-α/TNFR superfamily 1A signaling can affect T cell biology, focusing on conventional CD4+CD25− and regulatory CD4+CD25+ T cell functions in patients with TNFR-associated periodic syndrome carrying either high or low penetrance TNFRSF1A mutations. Specifically, we observed that in high penetrance TNFR-associated periodic syndrome, at the molecular le…

Male0301 basic medicinePenetranceAutoimmunitymedicine.disease_causeT-Lymphocytes RegulatoryImmune toleranceSettore MED/38 - Pediatria Generale E SpecialisticaTRAPS; Tconvs; Tregs; autoimmunity; immune toleranceImmunology and AllergyIL-2 receptorChildGeneticsMutationTconvTOR Serine-Threonine Kinaseshemic and immune systemsMiddle AgedAcquired immune systemPenetranceTregSTAT Transcription Factorsmedicine.anatomical_structureReceptors Tumor Necrosis Factor Type ICytokinesFemalebiological phenomena cell phenomena and immunitySignal TransductionAdultAdolescentFeverT cellAutoimmunity; Immune tolerance; Tconvs; Tregs; TRAPS; Cell Biology; ImmunologyImmunologyReceptors Antigen T-CellContext (language use)Tregs[object Object]BiologyImmunophenotypingYoung Adult03 medical and health sciencesImmune systemmedicineHumansAgedCell ProliferationDemographyTconvsImmune toleranceHereditary Autoinflammatory DiseasesTRAPSCell Biologybiological factors030104 developmental biologyMutationCancer research
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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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Common extracellular matrix regulation of myeloid cell activity in the bone marrow and tumor microenvironments

2017

The complex interaction between cells undergoing transformation and the various stromal and immunological cell components of the tumor microenvironment (TME) crucially influences cancer progression and diversification, as well as endowing clinical and prognostic significance. The immunosuppression characterizing the TME depends on the recruitment and activation of different cell types including regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. Less considered is the non-cellular component of the TME. Here, we focus on the extracellular matrix (ECM) regulatory activities that, within the TME, actively contribute to many aspects of tumor progression, acti…

0301 basic medicineCancer ResearchCell typeStromal cellMyeloidCarcinogenesisImmunologyBiology03 medical and health sciencesBone MarrowNeoplasmsmedicineImmune ToleranceImmunology and AllergyAnimalsHumansMyeloid-Derived Suppressor CellCarcinogenesiTumor microenvironmentAnimalMyeloid-Derived Suppressor CellsHematopoietic stem cellSPARCBone marrow nicheExtracellular matrixCell biology030104 developmental biologymedicine.anatomical_structureRegulatory myeloid suppressor cellOncologyTumor microenvironmentTumor progressionMyeloid-derived Suppressor CellBone marrow niche; Extracellular matrix; Regulatory myeloid suppressor cells; SPARC; Tumor microenvironment; Animals; Bone Marrow; Carcinogenesis; Extracellular Matrix; Humans; Immune Tolerance; Myeloid-Derived Suppressor Cells; Neoplasms; Tumor Escape; Tumor MicroenvironmentNeoplasmTumor Escapesense organsBone marrowHuman
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Immune tolerance induction with moroctocog-alpha (Refacto/Refacto AF) in a population of Italian haemophilia A patients with high-titre inhibitors: D…

2019

Background: The appearance of inhibitors is the most serious complication in haemophilia A (HA) patients. The primary objective is their eradication. Up to date, immune tolerance induction (ITI) was the only therapeutic option to achieve this. Aim: To assess the efficacy of moroctocog-alpha as an ITI regimen in a population of HA patients with high-titre inhibitors. Methods: The REF.IT Registry is a retrospective-prospective study that collected data on all patients with HA and high-titre inhibitors treated with moroctocog-alpha as an ITI regimen at twelve Italian Haemophilia Centres. Results: We enrolled 27 patients, 85.2% were children. All patients were high responders, 88.9% had severe …

AdultMalemedicine.medical_specialtyPopulationHaemophilia AAlpha (ethology)030204 cardiovascular system & hematologyHaemophiliaHemophilia Ahaemophilia A with inhibitors; immune tolerance induction; moroctocog-alpha; poor-prognosis ITI patients; Adult; Child; Child Preschool; Factor VIII; Female; Hemophilia A; Humans; Immune Tolerance; Italy; Male; Prospective Studies; Retrospective Studies; Risk Factors; RegistriesImmune tolerance03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicineImmune ToleranceMedicineHumansProspective StudiesRegistrieseducationHigh titrePreschoolChildGenetics (clinical)Retrospective Studiesimmune tolerance inductioneducation.field_of_studyFactor VIIIbusiness.industryHematologyGeneral Medicinehaemophilia A with inhibitormedicine.diseasepoor-prognosis ITI patientsRegimenItalymoroctocog-alphaChild PreschoolFemalebusinessComplicationhaemophilia A with inhibitors030215 immunologyHaemophilia : the official journal of the World Federation of HemophiliaREFERENCES
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Extracellular Vesicles and Tumor-Immune Escape: Biological Functions and Clinical Perspectives

2020

The modulation of the immune system is one of the hallmarks of cancer. It is now widely described that cancer cells are able to evade the immune response and thus establish immune tolerance. The exploration of the mechanisms underlying this ability of cancer cells has always attracted the scientific community and is the basis for the development of new promising cancer therapies. Recent evidence has highlighted how extracellular vesicles (EVs) represent a mechanism by which cancer cells promote immune escape by inducing phenotypic changes on different immune cell populations. In this review, we will discuss the recent findings on the role of tumor-derived extracellular vesicles (TEVs) in re…

animal diseasesCellProgrammed Cell Death 1 Receptorchemical and pharmacologic phenomenapd-1/pd-l1 axisReviewBiologyCatalysisImmune toleranceInorganic Chemistrylcsh:ChemistryExtracellular VesiclesImmune systemNeoplasmsmedicineImmune ToleranceAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyMechanism (biology)Organic ChemistryCancerGeneral Medicinebiochemical phenomena metabolism and nutritionimmune checkpointsmedicine.diseasePhenotypeComputer Science ApplicationsCell biologyextracellular vesicles (evs) cancer immune toleranceThe Hallmarks of Cancermedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Cancer cellbacteriaTumor EscapeImmune checkpointImmunotherapyextracellular vesicles (EVs)cancer immune toleranceInternational Journal of Molecular Sciences
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