Search results for " Mast Cells"

showing 10 items of 17 documents

Mast Cells and Th17 Cells Contribute to the Lymphoma-Associated Pro-Inflammatory Microenvironment of Angioimmunoblastic T-Cell Lymphoma

2010

Reports focusing on the immunological microenvironment of peripheral T-cell lymphomas (PTCL) are rare. Here we studied the reciprocal contribution of regulatory (Treg) and interleukin-17-producing (Th17) T-cells to the composition of the lymphoma-associated microenvironment of angioimmunoblastic T-cell lymphoma (AITL) and PTCL not otherwise specified on tissue microarrays from 30 PTCLs not otherwise specified and 37 AITLs. We found that Th17 but not Treg cells were differently represented in the two lymphomas and correlated with the amount of mast cells (MCs) and granulocytes, which preferentially occurred in the cellular milieu of AITL cases. We observed that MCs directly synthesized inter…

Angioimmunoblastic T-cell lymphomaLymphomaInflammationBiologymedicine.disease_causeCXCR3Lymphoma T-CellCXCR5Pathology and Forensic MedicineAutoimmunityAnimals Chemokine CXCL13; immunology Cytokines; genetics/immu/nology Forkhead Transcription Factors; immunology Gene Expression Profiling Humans Immunoblastic Lymphadenopathy; immunology/pathology Inflammation; immunology Interleukin-17; immunology Interleukin-6; immunology Lymphoma; T-Cell; immunology/pathology Mast Cells; immunology Microarray Analysis Th17 Cells; immunology Tumor MicroenvironmentimmunologymedicineTumor MicroenvironmentAnimalsHumansMast CellsInflammationTumor microenvironmentInterleukin-6Gene Expression ProfilingInterleukin-17Forkhead Transcription FactorsMast cellmedicine.diseaseT-CellMicroarray AnalysisChemokine CXCL13humanitiesgenetics/immu/nologyLymphomamedicine.anatomical_structureImmunoblastic LymphadenopathyImmunologyCytokinesimmunology/pathologyTh17 CellsMast Cell microenvironment angioimmunoblasticmedicine.symptomRegular Articles
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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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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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Mast cells crosstalk with B cells in the gut and sustain IgA response in the inflamed intestine.

2021

B lymphocytes are among the cell types whose effector functions are modulated by mast cells (MCs). The B/MC crosstalk emerged in several pathological settings, notably the colon of inflammatory bowel disease (IBD) patients is a privileged site in which MCs and IgA+ cells physically interact. Herein, by inducing conditional depletion of MCs in red MC and basophil (RMB) mice, we show that MCs control B cell distribution in the gut and IgA serum levels. Moreover, in dextran sulfate sodium (DSS)-treated RMB mice, the presence of MCs is fundamental for the enlargement of the IgA+ population in the bowel and the increase of systemic IgA production. Since both conventional B-2 and peritoneal-deriv…

0301 basic medicineCell typeColon[SDV]Life Sciences [q-bio]ImmunologyPopulationInflammationBasophilBiologySettore MED/08 - Anatomia Patologicabehavioral disciplines and activitiesInflammatory bowel diseasecell-to-cell interplay colitis IgAinnate-like B cells mast cells03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsMast CellsColitisIntestinal MucosaeducationB cellComputingMilieux_MISCELLANEOUSInflammationeducation.field_of_studyB-LymphocytesTumor Necrosis Factor-alphaDextran Sulfatemedicine.diseaseColitisInflammatory Bowel DiseaseshumanitiesInnate-like B cellsGastrointestinal MicrobiomeImmunoglobulin AMice Inbred C57BLCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureCell-to-cell interplayCell-to-cell interplay; Colitis; IgA; Innate-like B cells; Mast cellsImmunologymedicine.symptomIgA030215 immunologyEuropean journal of immunologyReferences
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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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The Anti-apoptotic Murine Cytomegalovirus Protein vMIA-m38.5 Induces Mast Cell Degranulation.

2020

Mast cells (MC) represent "inbetweeners" of the immune system in that they are part of innate immunity by acting as first-line sentinels for environmental antigens but also provide a link to adaptive immunity by secretion of chemokines that recruit CD8 T cells to organ sites of infection. An interrelationship between MC and cytomegalovirus (CMV) has been a blank area in science until recently when the murine model revealed a role for MC in the resolution of pulmonary infection by murine CMV (mCMV). As to the mechanism, MC were identified as a target cell type of mCMV. Infected MC degranulate and synthesize the CC-chemokine ligand-5 (CCL-5), which is released to attract protective virus-spec…

0301 basic medicineMicrobiology (medical)Chemokinebone marrow-derived mast cells (BMMC)Muromegalovirusmurine cytomegalovirus030106 microbiologyImmunologygene m38.5lcsh:QR1-502CytomegalovirusApoptosisInhibitor of apoptosisMicrobiologylcsh:MicrobiologyCell Degranulation03 medical and health sciencesMiceImmune systemCellular and Infection MicrobiologyCytotoxic T cellAnimalsperitoneal exudate-derived mast cells (PEMC)Mast CellsdegranulationInnate immune systembiologyDegranulationvirus diseasesTransfectionBrief Research ReportAcquired immune systemCell biologyvMIA030104 developmental biologyInfectious Diseasesbiology.proteinmast cell-specific Cre recombinationApoptosis Regulatory ProteinsFrontiers in cellular and infection microbiology
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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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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 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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Tumor-intrinsic and -extrinsic roles of c-Kit: mast cells as the primary off-target of tyrosine kinase inhibitors.

2011

c-Kit tyrosine kinase receptor and its ligand stem cell factor have multiple functions during development, whereas in adulthood they are mostly needed for stem cell (SC) maintenance and mast cell (MC) biology. c-Kit plays an essential tumor-cell-intrinsic role in many types of cancer, either providing the tumorigenic force when aberrantly activated or conferring stem-like features characterizing the most aggressive variants. A tumor-cell-extrinsic role occurs through c-Kit-dependent accessory cells (such as MCs) that infiltrate tumors and deeply influence their progression. c-Kit-targeted therapy with tyrosine kinase inhibitors (TKIs) may ideally work against both tumor and stromal cells. H…

Cancer ResearchStromal cellStem cell factorAntineoplastic AgentsBiologyc-kit; mast cells; mouse mutants; off-target; tyrosine kinase inhibitorsReceptor tyrosine kinaseMicec-KitNeoplasmstyrosine kinase inhibitorsGeneticsmedicineAnimalsHumansNeoplasm InvasivenessMast CellsMolecular BiologyProtein Kinase InhibitorsStem Cell Factormouse mutantsNeovascularization PathologicMast cellRatsProto-Oncogene Proteins c-kitmedicine.anatomical_structureTumor progressionmast cells.biology.proteinCancer researchStem cellTyrosine kinasePlatelet-derived growth factor receptoroff-targetMastocytosisOncogene
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