Search results for " Immunology"

showing 10 items of 1841 documents

Reciprocal influence of B cells and tumor macro and microenvironments in the ApcMin/+ model of colorectal cancer

2017

One of the most fascinating aspects of the immune system is its dynamism, meant as the ability to change and readapt according to the organism needs. Following an insult, we assist to the spontaneous organization of different immune cells which cooperate, locally and at distance, to build up an appropriate response. Throughout tumor progression, adaptations within the systemic tumor environment, or macroenvironment, result in the promotion of tumor growth, tumor invasion and metastasis to distal organs, but also to dramatic changes in the activity and composition of the immune system. In this work, we show the changes of the B-cell arm of the immune system following tumor progression in the…

lcsh:Immunologic diseases. Allergy0301 basic medicineColorectal cancerImmunologySpleenintestinal cancerBiologylcsh:RC254-282Metastasis03 medical and health sciencesImmune systemPeritoneummedicineImmunology and Allergyapcmin/+ miceApcMin/+mice; B lymphocytes; IgA; IL-10; intestinal cancer; Immunology and Allergy; Immunology; OncologyB lymphocyteApcMin/+micelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePhenotypeInterleukin 10030104 developmental biologymedicine.anatomical_structureOncologyTumor progressionIL-10Immunologyb lymphocyteslcsh:RC581-607IgAOncoImmunology
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Complement Protein C1q Binds to Hyaluronic Acid in the Malignant Pleural Mesothelioma Microenvironment and Promotes Tumor Growth

2017

C1q is the first recognition subcomponent of the complement classical pathway, which acts towards the clearance of pathogens and apoptotic cells. C1q is also known to modulate a range of functions of immune and non-immune cells, including their involvement in placental development and sensorial synaptic pruning. We have recently shown that C1q can promote tumour by encouraging their adhesion, migration and proliferation in addition to angiogenesis and metastasis. In this study, we have examined the role of C1q in the microenvironment of malignant pleuric mesothelioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. We found that C1q was highly expressed in all MPM…

lcsh:Immunologic diseases. Allergy0301 basic medicineComplement system; Malignant pleural mesothelioma; Hyaluronic acid; Mesothelioma cells; C1q; CancerAngiogenesisMPMp38 mitogen-activated protein kinasesImmunologyHAchemical and pharmacologic phenomenaBiologyMetastasisMesothelioma cell03 medical and health sciencesClassical complement pathwaychemistry.chemical_compound0302 clinical medicineImmune systemhyaluronic acidHyaluronic acidmedicinemalignant pleural mesotheliomacancerImmunology and AllergyCell adhesioncomplement systemC1qcomplement system; MPM; HA; Mesothelioma cells; C1q and cancerOriginal ResearchC1q and cancermedicine.diseaseComplement system030104 developmental biologyC1q; Cancer; Complement system; Hyaluronic acid; Malignant pleural mesothelioma; Mesothelioma cells; Immunology and Allergy; Immunologychemistrymesothelioma cells030220 oncology & carcinogenesisImmunologyCancer researchlcsh:RC581-607Frontiers in Immunology
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Macrophages as an Emerging Source of Wnt Ligands: Relevance in Mucosal Integrity

2019

The Wnt signaling pathway is a conserved pathway involved in important cellular processes such as the control of embryonic development, cellular polarity, cellular migration, and cell proliferation. In addition to playing a central role during embryogenesis, this pathway is also an essential part of adult homeostasis. Indeed, it controls the proliferation of epithelial cells in different organs such as intestine, lung, and kidney, and guarantees the maintenance of the mucosa in physiological conditions. The origin of this molecular pathway is the binding between Wnt ligands (belonging to a family of 19 different homologous secreted glycoproteins) and their specific membrane receptors, from …

lcsh:Immunologic diseases. Allergy0301 basic medicineFrizzledCellular polarityImmunologyReviewmacrophageBiologyLigandsProinflammatory cytokine03 medical and health sciencesParacrine signalling0302 clinical medicineNeoplasmsWnt ligandsmucosal homeostasisHumanscancerImmunology and AllergyAutocrine signallingWnt Signaling PathwayInflammationMucous MembraneInnate immune systemMacrophagesfibrosisWnt signaling pathwayCell migrationImmunity InnateCell biologyWnt Proteins030104 developmental biologyregenerationlcsh:RC581-607Protein Binding030215 immunologyFrontiers in Immunology
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F-Type Lectins: A highly diversified family of fucose-binding proteins with a unique sequence motif and structural fold, involved in self/non-self-re…

2017

The F-type lectin (FTL) family is one of the most recent to be identified and structurally characterized. Members of the FTL family are characterized by a fucose recognition domain [F-type lectin domain (FTLD)] that displays a novel jellyroll fold (“F-type” fold) and unique carbohydrate- and calcium-binding sequence motifs. This novel lectin family comprises widely distributed proteins exhibiting single, double, or greater multiples of the FTLD, either tandemly arrayed or combined with other structurally and functionally distinct domains, yielding lectin subunits of pleiotropic properties even within a single species. Furthermore, the extraordinary variability of FTL sequences (isoforms) th…

lcsh:Immunologic diseases. Allergy0301 basic medicineGene isoformImmunologySettore BIO/05 - ZoologiaFucose bindingReviewFucoseF-type lectinsSelf/non-self-recognitionKelch motif03 medical and health scienceschemistry.chemical_compoundGene duplicationImmunology and AllergyStructural modelingGeneticsInnate immunitybiologyPhylogenetic treefucolectinsLectinGlycan recognition030104 developmental biologychemistrybiology.proteinFucose-bindingFucolectinlcsh:RC581-607Sequence motifF-type lectinF-type lectins; Fucolectins; Fucose-binding; Glycan recognition; Innate immunity; Self/non-self-recognition; Structural modeling; Immunology and Allergy; Immunology
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Pathogenic Role of Complement in Antiphospholipid Syndrome and Therapeutic Implications

2018

Antiphospholipid syndrome (APS) is an acquired autoimmune disease characterized by thromboembolic events, pregnancy morbidity, and the presence of antiphospholipid (aPL) antibodies. There is sound evidence that aPL act as pathogenic autoantibodies being responsible for vascular clots and miscarriages. However, the exact mechanisms involved in the clinical manifestations of the syndrome are still a matter of investigation. In particular, while vascular thrombosis is apparently not associated with inflammation, the pathogenesis of miscarriages can be explained only in part by the aPL-mediated hypercoagulable state and additional non-thrombotic effects, including placental inflammation, have b…

lcsh:Immunologic diseases. Allergy0301 basic medicineImmunologyComplementMiscarriagesAnti-beta2 glycoprotein I antibodieInflammationMiscarriagePathogenesis03 medical and health sciences0302 clinical medicineImmune systemAntiphospholipid syndromeimmune system diseasesAntiphospholipid syndromeMedicineImmunology and AllergyAnimal model030203 arthritis & rheumatologyAutoimmune diseaseInflammationbusiness.industryAutoantibodyThrombosismedicine.diseaseComplement (complexity)Complement systemAnimal models030104 developmental biologyAnti-beta2 glycoprotein I antibodiesPerspectiveThrombosiImmunologyAnimal models; Anti-beta2 glycoprotein I antibodies; Antiphospholipid syndrome; Complement; Inflammation; Miscarriages; Therapy; Thrombosis; Immunology and Allergy; ImmunologyTherapymedicine.symptomlcsh:RC581-607businessFrontiers in Immunology
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The prognostic and predictive value of IKZF1 and IKZF3 expression in T-cells in patients with multiple myeloma

2018

Purpose: While recent studies described the role of IKZF1/3 proteins in multiple myeloma (MM) cells, few have highlighted the significance of IKZF1/3 expression in T-cells. In this study we examine the prognostic and predictive value of IKZF1/3 expression in T-cells in patients with MM stage III. Experimental design: We analysed the IKZF1/3 expression levels in T-cells from 45 MM stage I (MMI) and 50 newly diagnosed MM stage III (MMIII) patients, according to Durie-Salmon staging system, by flow cytometry to examine their prognostic and predictive value. We also combined in vivo observations with in vitro assays to determine the effect of IKZF1/3 expression on the T-cell immunophenotype and…

lcsh:Immunologic diseases. Allergy0301 basic medicineOncologymedicine.medical_specialtyImmunologyMedizinlcsh:RC254-282Flow cytometry03 medical and health sciencesikzf10302 clinical medicineImmunophenotypingikzf3immunomodulatory drugsIn vivoInternal medicinemedicineImmunology and AllergyStage (cooking)t cellsMultiple myelomaOriginal ResearchLenalidomidemedicine.diagnostic_testbusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePomalidomidemultiple myelomaThalidomide030104 developmental biologyOncologybiomarker trialsimmunelcsh:RC581-607business030215 immunologymedicine.drug
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Azithromycin Differentially Alters TCR-Activated Helper T Cell Subset Phenotype and Effector Function

2020

In addition to their antibiotic activities, azithromycin (AZM) exhibits anti-inflammatory effects in various respiratory diseases. One of the potent anti-inflammatory mechanisms is through inhibition of CD4+ helper T (Th) cell effector function. However, their impact on specific Th subset is obscure. Herein, we demonstrate the cellular basis of phenotypic and functional alterations associated with Th subsets following AZM treatment in vitro. Using well-characterized Th subset specific chemokine receptors, we report significant suppression of T cell receptor (TCR)-stimulated hyperactivated CCR4+CXCR3+ (Th0) expansion compared to CCR4-CXCR3+ (Th1-like) and CCR4+CXCR3- (Th2-like) cells. Intere…

lcsh:Immunologic diseases. Allergy0301 basic medicineReceptors CCR4Receptors CXCR3Receptor expressionImmunologyReceptors Antigen T-CellBiologyCXCR303 medical and health sciencesChemokine receptorInterferon-gamma0302 clinical medicineDownregulation and upregulationCell MovementT-Lymphocyte SubsetsImmunology and AllergyHumansIFN-γInterleukin 4Cells CulturedOriginal Researchanti-inflammatoryazithromycinCD4+ helper T cellsCXCR3EffectorCell growthT-cell receptorIL-4apoptosisCell DifferentiationBacterial InfectionsTh1 CellsHealthy VolunteersCell biologyAnti-Bacterial Agents030104 developmental biologyCCR4Interleukin-4lcsh:RC581-607030215 immunologyFrontiers in Immunology
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Baseline Gut Microbiota Composition Is Associated With Schistosoma mansoni Infection Burden in Rodent Models

2020

In spite of growing evidence supporting the occurrence of complex interactions between Schistosoma and gut bacteria in mice and humans, no data is yet available on whether worm-mediated changes in microbiota composition are dependent on the baseline gut microbial profile of the vertebrate host. In addition, the impact of such changes on the susceptibility to, and pathophysiology of, schistosomiasis remains largely unexplored. In this study, mice colonized with gut microbial populations from a human donor (HMA mice), as well as microbiota-wild type (WT) animals, were infected with Schistosoma mansoni, and alterations of their gut microbial profiles at 50 days post-infection were compared to …

lcsh:Immunologic diseases. Allergy0301 basic medicineRodentImmunologyAntibodies ProtozoanSchistosomiasisGut floradigestive systemParasite LoadHost-Parasite InteractionsMicrobiologyImmunomodulationFecesMice03 medical and health sciences0302 clinical medicineimmune-modulationhuman-microbiota associated mouse modelsRNA Ribosomal 16Sbiology.animalLactobacillusmedicineAnimalsImmunology and AllergySchistosomaBacteriabiologyFOS: Clinical medicineComputational BiologyBiodiversitySchistosoma mansonidysbiosismedicine.diseasebiology.organism_classificationSchistosomiasis mansoniGastrointestinal MicrobiomeDisease Models Animal030104 developmental biologyhelminth-gut microbiota interactionsSchistosomaMetagenomicsSchistosoma mansonigut microbial diversityProteobacterialcsh:RC581-607Dysbiosis030215 immunology
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Candida spp. Determination and Th1/Th2 Mixed Cytokine Profile in Oral Samples From HIV+ Patients With Chronic Periodontitis

2019

Background: Chronic periodontitis (CP), caused by bacteria and fungi, appears in up to 66% of HIV-patients. The impact and association of HIV-treatment (HAART) and Candida itself has not been properly evaluated in the development and progression of CP. The immunopathogenesis is characterized by CD4+ T-cells activation and the balance between the T-helper 1 (Th1) and T-helper 2 (Th2) or a mixed cytokine profile. Currently, the associated causes of an immune response in HIV-patients with CP is controversial. Our aims were the determination of Candida spp. and cytokine profile in oral samples from HIV-positive patients with CP, considering the CD4+ T cells levels and HAART use.Methods: From 50…

lcsh:Immunologic diseases. Allergy0301 basic medicineSalivaHAARTmedicine.medical_treatmentImmunologyGroup AGroup BMicrobiology03 medical and health sciences0302 clinical medicinemedicineImmunology and AllergyOriginal ResearchCandida sppmedicine.diagnostic_testbusiness.industryHIVchronic periodontitisImmunosuppressionmedicine.diseaseChronic periodontitiscytokinesCorpus albicans030104 developmental biologyCytokineImmunoassaylcsh:RC581-607business030215 immunologyFrontiers in Immunology
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A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets.

2018

International audience; NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR(B6C14R) strain. Ly5.1(C14R) NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46(C14R) in 293T cells showed that NKp46 protein trafficking to the cell surface …

lcsh:Immunologic diseases. Allergy0301 basic medicineSignal peptideintracellular traffickingImmunologyCellCongenicinnate lymphoid cellsBiologymedicine.disease_causelcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineImmunology and Allergyddc:610congenic miceReceptorOriginal ResearchMutationEndoplasmic reticulumInnate lymphoid cellHEK 293 cellslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCell biology030104 developmental biologymedicine.anatomical_structureOncologyactivation receptors[SDV.IMM]Life Sciences [q-bio]/Immunologylcsh:RC581-607030215 immunology
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