Search results for " mast cells"

showing 7 items of 17 documents

Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers

2011

Abstract Mast cells (MC) are c-Kit–expressing cells, best known for their primary involvement in allergic reactions, but recently reappraised as important players in either cancer promotion or inhibition. Here, we assessed the role of MCs in prostate tumor development. In prostate tumors from both tumor-prone transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and human patients, MCs are specifically enriched and degranulated in areas of well-differentiated (WD) adenocarcinoma but not around poorly differentiated (PD) foci that coexist in the same tumors. We derived novel TRAMP tumor cell lines, representative of WD and PD variants, and through pharmacologic stabilization or geneti…

MaleOncologyCancer Researchmedicine.medical_specialtyEpithelial-Mesenchymal TransitionMice TransgenicAdenocarcinomaBiologymedicine.disease_causeCell DegranulationMiceProstate cancerProstateCell Line TumorInternal medicineTumor MicroenvironmentmedicineMast CellAnimalsHumansMast CellsReceptors Tumor Necrosis Factor Member 25Tumor microenvironmentAdenocarcinoma; Animals; Carcinoma Neuroendocrine; Cell Degranulation; Cell Line Tumor; Disease Progression; Epithelial-Mesenchymal Transition; Humans; Male; Mast Cells; Matrix Metalloproteinase 9; Mice; Mice Inbred C57BL; Mice Transgenic; Prostatic Neoplasms; Proto-Oncogene Proteins c-kit; Receptors Tumor Necrosis Factor Member 25; Tumor Microenvironment; Cancer Research; OncologyAnimalProstatic NeoplasmsCancermedicine.diseasehumanitiesCarcinoma NeuroendocrineMice Inbred C57BLProto-Oncogene Proteins c-kitmedicine.anatomical_structureMatrix Metalloproteinase 9OncologyTumor progressionProstatic NeoplasmDisease ProgressionAdenocarcinomaCarcinogenesisHumanTramp
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INFLAMMATION IN IRRITABLE BOWEL SYNDROME: MYTH OR NEW TREATMENT TARGET?

2016

Low-grade intestinal inflammation plays a key role in the pathophysiology of irritable bowel syndrome (IBS), and this role is likely to be multifactorial. The aim of this review was to summarize the evidence on the spectrum of mucosal inflammation in IBS, highlighting the relationship of this inflammation to the pathophysiology of IBS and its connection to clinical practice. We carried out a bibliographic search in Medline and the Cochrane Library for the period of January 1966 to December 2014, focusing on publications describing an interaction between inflammation and IBS. Several evidences demonstrate microscopic and molecular abnormalities in IBS patients. Understanding the mechanisms u…

Pathologymedicine.medical_specialtyMEDLINEAnti-Inflammatory AgentsInflammationCochrane LibraryBioinformaticsMast cell03 medical and health sciences0302 clinical medicineTreatment targetsGastrointestinal AgentsIntestinal inflammationmedicinePathologyAnimalsHumansMolecular Targeted TherapyTopic HighlightIntestinal MucosaIrritable bowel syndromeInflammationSettore MED/12 - GastroenterologiaMechanism (biology)business.industrySettore BIO/16 - Anatomia UmanaGastroenterologyGeneral MedicineInflammation; Irritable bowel syndrome; Mast cells; Neuroendocrine cells; Pathologymedicine.diseaseEnteritisClinical trialIrritable bowel syndromeSettore MED/18 - Chirurgia Generale030220 oncology & carcinogenesisNeuroendocrine cell030211 gastroenterology & hepatologymedicine.symptomInflammation Mediatorsbusiness
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Mast cells in canine mammary gland tumour: number, distribution and EPOR positivity.

2011

Erythropoietin (EPO)-mediated mitogenic and anti-apoptotic effects involve all the cells expressing functional receptors for EPO (EPOR), as demonstrated by in vitro and in vivo studies. EPO shows pleiotropic effects and acts as an endogenous mediator of adaptive tissue response to metabolic stress protecting tissues from different injuries. Recently, the EPO/EPOR complex has been identified in several neoplastic cell lines and solid tumours. In this study, the authors investigated the mast cells (MCs) number, distribution and their immunoreactivity for EPOR in normal, dysplastic and neoplastic canine mammary gland. The results showed that MCs were more numerous in displastic glands compared…

Pathologymedicine.medical_specialtyMammary glandMammary glanddog; erythropoietin; mast cellsMammary Neoplasms Animalmast cellsBiologymedicine.disease_causeMast cellDogsEPO EPORmedicineAnimalsDog DiseasesReceptorSchools VeterinaryGeneral VeterinaryAnimalSettore MED/27 - NeurochirurgiaEPORfood and beveragesImmunohistochemistryEpitheliumErythropoietin receptormedicine.anatomical_structureOncologyItalySettore VET/03 - Patologia Generale E Anatomia Patologica VeterinariaErythropoietinembryonic structuresdogVeterinary (all)ImmunohistochemistryNeoplastic cellFemaleerythropoietinDog DiseaseCarcinogenesismedicine.drug
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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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CD4+CD25+ regulatory T cells suppress mast cell degranulation and allergic responses through OX40-OX40L interaction.

2008

T regulatory (Treg) cells play a role in the suppression of immune responses, thus serving to induce tolerance and control autoimmunity. Here, we explored whether Treg cells influence the immediate hypersensitivity response of mast cells (MCs). Treg cells directly inhibited the FcεRI-dependent MC degranulation through cell-cell contact involving OX40-OX40L interactions between Treg cells and MCs, respectively. When activated in the presence of Treg cells, MCs showed increased cyclic adenosine monophosphate (cAMP) concentrations and reduced Ca2+ influx, independently of phospholipase C (PLC)-γ2 or Ca2+ release from intracellular stores. Antagonism of cAMP in MCs reversed the inhibitory effec…

T-LymphocytesCELLIMMUNO; Animals; Calcium; Cell Line Tumor; Gene Knockdown Techniques; Histamine Release; Humans; Hypersensitivity; Mast Cells; Membrane Glycoproteins; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Phospholipase C gamma; Receptors OX40; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Cell Degranulation; Immunology and Allergy; Infectious Diseases; ImmunologyInbred C57BLmedicine.disease_causeHistamine ReleaseT-Lymphocytes RegulatoryCell DegranulationAutoimmunityMicechemistry.chemical_compoundReceptorsImmunology and AllergyOX40Mast CellsInbred BALB CMice Inbred BALB CTumorMembrane GlycoproteinsDegranulationhemic and immune systemsRegulatoryhumanitiesCell biologyTregInfectious DiseasesGene Knockdown TechniquesTumor Necrosis FactorsMembrane GlycoproteinMast cell; Treg; OX40-OX40L interactionIntracellularHumanCell DegranulationImmunologyInfectious Diseasechemical and pharmacologic phenomenaBiologybehavioral disciplines and activitiesArticleCell LineMast cellImmune systemCell Line TumorHypersensitivitymedicineAnimalsHumansCyclic adenosine monophosphatePhospholipase CAnimalPhospholipase C gammaReceptors OX40Mice Inbred C57BLchemistryCELLIMMUNOCell cultureGene Knockdown TechniqueImmunologyOX40-OX40L interactionCalciumTumor Necrosis Factor
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis

2021

Copyright © 2021 Agostinis, Zorzet, Balduit, Zito, Mangogna, Macor, Romano, Toffoli, Belmonte, Morello, Martorana, Borelli, Ricci, Kishore and Bulla. The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against…

endometriosisTHP-1 CellsTNF-amast cellsPeritoneal DiseasesCell DegranulationEndometriumImmunology and AllergyOriginal ResearchMice Knockoutmedicine.diagnostic_testendometriosiComplement C3Hep G2 CellsAntibody opsonizationmedicine.anatomical_structureComplement C3aTumor necrosis factor alphaFemaleInflammation MediatorsSignal TransductionImmunologyBiologySettore MED/08 - Anatomia PatologicaImmunofluorescencePeritoneal cavityPeritoneummedicineAnimalsHumansSettore MED/05 - Patologia ClinicaC3complement system...Innate immune systemTumor Necrosis Factor-alphaPeritoneal fluidC3; endometriosis; mast cells; complement system; TNF-aRC581-607Coculture TechniquesImmunity InnateComplement systemImmunity HumoralMice Inbred C57BLDisease Models AnimalCase-Control StudiesTNF-αCancer researchPeritoneal DiseaseImmunologic diseases. Allergymast cell
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