Search results for " B-Cell"

showing 10 items of 207 documents

Mechanisms of the Development of Allergy (MeDALL) : Introducing novel concepts in allergy phenotypes

2017

Asthma, rhinitis, and eczema are complex diseases with multiple genetic and environmental factors interlinked through IgE-associated and non–IgE-associated mechanisms. Mechanisms of the Development of ALLergy (MeDALL; EU FP7-CP-IP; project no: 261357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels by linking epidemiologic, clinical, and mechanistic research, including in vivo and in vitro models. MeDALL integrated 14 European birth cohorts, including 44,010 participants and 160 cohort follow-ups between pregnancy and age 20 years. Thirteen thousand children were prospectively followed after puberty by using a newly standardized MeDALL Core Q…

0301 basic medicineAllergyGenome-wide association studyComorbidityImmunoglobulin Emedicine.disease_causeCohort StudiesTranslational Research Biomedical0302 clinical medicineAllergenREGULATORY B-CELLSPRECISION MEDICINEMedicineBIRTH COHORT INFANTSATOPIC-DERMATITISImmunology and Allergy[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/AllergologyChildmedia_commonbiologyatopic dermatitisAtopic dermatitis3. Good healthEuropeMulticenter StudyCHRONIC RESPIRATORY-DISEASESrhinitiPhenotypeINNER-CITY CHILDRENBiomarker (medicine)Femaleatopic dermatitiAdolescentEUROPEAN INNOVATION PARTNERSHIPImmunologyreview03 medical and health sciencesEARLY-LIFEYoung AdultrhinitisAllergy ; Asthma ; Atopic Dermatitis ; RhinitisHypersensitivityJournal Articlemedia_common.cataloged_instanceAnimalsHumansEuropean unionAsthmaMOUNTAIN CEDAR POLLINOSISbusiness.industryGene Expression ProfilingCHILDHOOD ASTHMAAllergensImmunoglobulin Emedicine.diseaseallergyAsthma030104 developmental biology030228 respiratory systemImmunologybiology.proteinImmunizationbusinessGenome-Wide Association StudyJournal of Allergy and Clinical Immunology
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Checkpoint Inhibition in Non-Hodgkin's Lymphoma.

2017

As patients continue to die from malignant lymphoma, novel treatment options continue to be warranted. To successfully grow and spread, tumor cells need to escape the immune system; therefore, the augmentation or restoration of immune effectors against the malignant cell could be of great value, as shown, e.g., for allogeneic transplantation. A deepened understanding of the regulation of activation and inhibition of the T cell-based effector mechanisms has led to the development of drugs that are able to modify specific checkpoints of this system and thereby raise an immune response against tumor cells. With dramatic responses observed in Hodgkin's disease (HD), interest has risen to explor…

0301 basic medicineCancer ResearchAllogeneic transplantationT cellT-LymphocytesAntineoplastic AgentsDisease03 medical and health sciences0302 clinical medicineImmune systemhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineEffectorbusiness.industryLymphoma Non-HodgkinAntibodies MonoclonalHematologymedicine.diseaseIpilimumabLymphomaNon-Hodgkin's lymphoma030104 developmental biologymedicine.anatomical_structureNivolumabOncology030220 oncology & carcinogenesisCancer researchTumor EscapePrimary mediastinal B-cell lymphomabusinessRituximabOncology research and treatment
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Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

2017

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-l…

0301 basic medicineCancer ResearchTumor suppressor geneCell SurvivalRNA SplicingChronic lymphocytic leukemia2720 Hematology610 Medicine & healthBiologyCD5 Antigenslaw.inventionPathogenesisMice03 medical and health sciencesimmune system diseaseslawhemic and lymphatic diseasesmedicineAnimalsHumans10239 Institute of Laboratory Animal Science1306 Cancer ResearchGenes Tumor SuppressorGeneCell ProliferationB-LymphocytesAlternative splicingNF-kappa BUbiquitinationHematologymedicine.diseaseLeukemia Lymphocytic Chronic B-CellDeubiquitinating Enzyme CYLDLeukemia030104 developmental biologyOncologyImmunologyCancer research570 Life sciences; biologySuppressor2730 OncologyCD5Signal TransductionLeukemia
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Chimeric Antigen Receptor-Engineered T-Cells - A New Way and Era for Lymphoma Treatment.

2019

Background: Patients with refractory or relapsed diffuse large B-cell lymphoma have a poor prognosis with the current standard of care. Objective: Chimeric Antigen Receptor T-cells (CAR T-cells) are functionally reprogrammed lymphocytes, which are able to recognize and kill tumor cells. The aim of this study is to make progress in this area. Method: A mini-review was achieved using the articles published in Web of Science and PubMed in the last year and the new patents were made in this field. Results: The responses to CAR T-cell products axicabtagene ciloleucel and tisagenlecleucel are promising; the objective response rate can reach up to 83%, and the complete response rate ranges betwee…

0301 basic medicineCancer Researchmedicine.drug_classmedicine.medical_treatmentT-LymphocytesMonoclonal antibodyImmunotherapy Adoptive03 medical and health sciences0302 clinical medicineInterferonDrug DiscoveryMedicineHumansPharmacology (medical)Clinical Trials as TopicReceptors Chimeric Antigenbusiness.industryGeneral MedicineImmunotherapymedicine.diseaseFusion proteinChimeric antigen receptorLymphomaCytokine release syndrome030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchLymphoma Large B-Cell DiffusebusinessDiffuse large B-cell lymphomamedicine.drugRecent patents on anti-cancer drug discovery
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A rare association of chronic lymphocytic leukemia with c-ANCA-positive Wegener’s granulomatosis: a case report

2016

Background Wegener’s granulomatosis is a systemic vasculitis of the small- and medium-sized vessels, produced by the action of ANCA, which involves the respiratory tract, kidneys, and eyes, with a potential for lethal evolution in the first year after diagnosis. Its association with chronic lymphocytic leukemia is rarely described in the literature, and it may be difficult to diagnose and to treat this association. Case presentation We present the case of a 73-year-old Caucasian patient, a rare case in which Wegener’s granulomatosis is associated in a patient with chronic lymphocytic leukemia, who is admitted in the Infectious Disease Department for fever, diplopia, headache, purulent and h…

0301 basic medicineChemosisMalePathologymedicine.medical_specialtyChronic lymphocytic leukemiaMucous membrane of noseCase ReportAntibodies Antineutrophil Cytoplasmic03 medical and health sciences0302 clinical medicineBiopsymedicinec-ANCA positiveHumansAgedmedicine.diagnostic_testbusiness.industryGranulomatosis with PolyangiitisWegener’s granulomatosismedicine.diseasePrognosisLeukemia Lymphocytic Chronic B-Cell030104 developmental biologyOncology030220 oncology & carcinogenesisChronic lymphocytic leukemiaSurgerymedicine.symptomGranulomatosis with polyangiitisVasculitisbusinessScleritisSystemic vasculitisWorld Journal of Surgical Oncology
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IL‐10‐producing B cells are characterized by a specific methylation signature

2019

Among the family of regulatory B cells, the subset able to produce interleukin-10 (IL-10) is the most studied, yet its biology is still a matter of investigation. The DNA methylation profiling of the il-10 gene locus revealed a novel epigenetic signature characterizing murine B cells ready to respond through IL-10 synthesis: a demethylated region located 4.5 kb from the transcription starting site (TSS), that we named early IL10 regulatory region (eIL10rr). This feature allows to distinguish B cells that are immediately prone and developmentally committed to IL-10 production from those that require a persistent stimulation to exert an IL-10-mediated regulatory function. These late IL-10 pro…

0301 basic medicineChronic lymphocytic leukemiaRegulatory B cellsImmunologyB-Lymphocyte SubsetsLymphoma Mantle-CellRegulatory Sequences Nucleic AcidBiologyLymphocyte ActivationB-cell malignanciesMice03 medical and health scienceschemistry.chemical_compoundInterleukin 100302 clinical medicineTranscription (biology)Immune ToleranceTumor MicroenvironmentmedicineAnimalsHumansImmunology and AllergyB cells; B-cell malignancies; DNA methylation; epigenetics; Interleukin 10; Immunology and Allergy; ImmunologyEpigeneticsB-Lymphocytes RegulatoryB cellsB cellDNA methylationepigeneticsGene Expression ProfilingB cells; B-cell malignancies; DNA methylation; epigenetics; Interleukin 10Cell DifferentiationMethylationmedicine.diseaseLeukemia Lymphocytic Chronic B-CellImmunity HumoralInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10030104 developmental biologychemistryDNA methylationB-cell malignancieFemaleepigeneticDNA030215 immunologyEuropean Journal of Immunology
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The IgG1 B-cell receptor provides survival and proliferative signals analogue to the Igα but not the Igβ co-receptor.

2016

The function of the IgM B-cell receptor (BCR) is dependent on intact signaling of the co-receptors Igα and Igβ, both of which contain a cytoplasmic tail bearing an immunoreceptor tyrosine-based activation motif. We have previously demonstrated that the cytoplasmic tail of the IgG1 BCR can partially compensate for the loss of the signaling moiety of Igα. Here, we show that unlike Igα, Igβ signaling is indispensable for the development and function of IgG1-expressing B cells. Deletion of the cytoplasmic signaling tail of Igβ compromised the survival and proliferation not only of IgM(+) B cells but also of IgG1-expressing B cells. In the absence of the signaling tail of Igβ, the transcription …

0301 basic medicineCo-receptorImmunologyB-cell receptorbcl-X ProteinReceptors Antigen B-CellBiologyCell Line03 medical and health sciencesTransduction (genetics)Mice0302 clinical medicineTranscription (biology)Immunology and AllergyAnimalsCyclin D2TyrosineReceptorCell ProliferationB-Lymphocytesbreakpoint cluster regionFlow CytometryCell biology030104 developmental biologyImmunoglobulin MCytoplasmImmunoglobulin GCancer researchCD79 Antigens030215 immunologySignal TransductionEuropean journal of immunology
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Intrasinusoidal HHV8-EBV–Positive Large B-Cell Lymphoma With Features of Germinotropic Lymphoproliferative Disorder

2020

Germinotropic lymphoproliferative disorder (GLPD) is a poorly characterized lymphoproliferative entity, recently included in the World Health Organization classification of hematolymphoid neoplasms. The histological pattern of this disease comprises monotypic plasmablasts that involve the germinal centers of the lymphoid follicles (germinotrophism), forming confluent aggregates positive for both human herpes virus type 8 (HHV8) and Epstein-Barr virus. Currently, after 17 years of its first description, only 18 cases have been reported. In this article, we describe a case of a GLPD presenting in an immunocompetent 79-year-old woman with localized axillary lymphadenopathy, showing a prominen…

0301 basic medicineEpstein-Barr Virus InfectionsHerpesvirus 4 HumanPathologymedicine.medical_specialtyLymphoma B-Cellmedicine.disease_causePathology and Forensic Medicine03 medical and health sciences0302 clinical medicinemedicineAxillary LymphadenopathyHumansB-cell lymphomaAnaplastic large-cell lymphomaAgedbusiness.industryGerminal centerHerpesviridae Infectionsmedicine.diseaseEpstein–Barr virusLymphoproliferative DisordersLymphoma030104 developmental biologyPleomorphism (cytology)030220 oncology & carcinogenesisHerpesvirus 8 HumanFemaleSurgeryLymph NodesAnatomyDifferential diagnosisbusinessInternational Journal of Surgical Pathology
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Regulatory T Cells in an Endogenous Mouse Lymphoma Recognize Specific Antigen Peptides and Contribute to Immune Escape.

2019

Abstract Foxp3+ regulatory T cells (Tregs) sustain immune homeostasis and may contribute to immune escape in malignant disease. As a prerequisite for developing immunologic approaches in cancer therapy, it is necessary to understand the ontogeny and the antigenic specificities of tumor-infiltrating Tregs. We addressed this question by using a λ-MYC transgenic mouse model of endogenously arising B-cell lymphoma, which mirrors key features of human Burkitt lymphoma. We show that Foxp3+ Tregs suppress antitumor responses in endogenous lymphoma. Ablation of Foxp3+ Tregs significantly delayed tumor development. The ratio of Treg to effector T cells was elevated in growing tumors, which could be …

0301 basic medicineGenetically modified mouseCancer ResearchLymphoma B-CellImmunologychemical and pharmacologic phenomenaMice TransgenicT-Lymphocytes RegulatoryEpitope03 medical and health sciences0302 clinical medicineAntigenCell Line TumorMHC class ImedicineAnimalsAntigensbiologyEffectorFOXP3hemic and immune systemsmedicine.diseaseLymphomaMice Inbred C57BL030104 developmental biologyTumor Escape030220 oncology & carcinogenesisCancer researchbiology.proteinTumor EscapePeptidesCancer immunology research
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HSP110 sustains chronic NF-κB signaling in activated B cell diffuse large B cell lymphoma through MyD88 stabilization

2018

International audience; Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) is an aggressive lymphoproliferative disorder involving chronic NF-κB activation. Several mutations in the BCR and the MyD88 signaling pathway components, such as MyD88 L265P, are implicated in this aberrant activation. Among heat-shock proteins, HSP110 has recently been identified as a pro- survival and/or proliferation factor in many cancers but its role in ABC-DLBCL survival mechanisms remained to be established. We observed that shRNA-mediated HSP110 silencing decreased the survival of several ABC-DLBCL cell lines, decreased IgM-MyD88 co-localization and subsequent NF-κB signaling. Conversely, over-expres…

0301 basic medicineImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/CancerCohort Studies03 medical and health sciencesimmune system diseaseshemic and lymphatic diseasesmedicineTumor Cells CulturedGene silencingHumansHSP110 Heat-Shock ProteinsB cellChemistryProtein StabilityWild typebreakpoint cluster regionNF-kappa BCell BiologyHematologymedicine.disease3. Good healthLymphoma030104 developmental biologymedicine.anatomical_structureCell cultureMyeloid Differentiation Factor 88Cancer researchLymphoma Large B-Cell DiffuseSignal transductionDiffuse large B-cell lymphomaSignal Transduction
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