Search results for "B-LYMPHOCYTE"

showing 10 items of 221 documents

Enhancement of cytotoxicity of artemisinins toward cancer cells by ferrous iron

2004

Abstract Iron(II) heme-mediated activation of the peroxide bond of artemisinins is thought to generate the radical oxygen species responsible for their antimalarial activity. We analyzed the role of ferrous iron in the cytotoxicity of artemisinins toward tumor cells. Iron(II)–glycine sulfate (Ferrosanol) and transferrin increased the cytotoxicity of free artesunate, artesunate microencapsulated in maltosyl-β-cyclodextrin, and artemisinin toward CCRF-CEM leukemia and U373 astrocytoma cells 1.5- to 10.3-fold compared with that of artemisinins applied without iron. Growth inhibition by artesunate and ferrous iron correlated with induction of apoptosis. Cell cycle perturbations by artesunate an…

ArtemisininsIronPopulationTransferrin receptorBiochemistryFerrousInhibitory Concentration 50chemistry.chemical_compoundAntigens CDCell Line TumorNeoplasmsPhysiology (medical)Receptors TransferrinHumansFerrous CompoundsRNA MessengereducationCell Proliferationchemistry.chemical_classificationeducation.field_of_studybiologyMolecular biologyArtemisininsAntigens Differentiation B-LymphocyteGene Expression RegulationBiochemistrychemistryTransferrinArtesunateCancer cellbiology.proteinTumor Suppressor Protein p53CeruloplasminFree Radical Biology and Medicine
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The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pa…

2006

We have recently demonstrated that the rheumatoid arthritis (RA) shared epitope (SE) acts as a ligand that triggers nitric oxide (NO) signaling in opposite cells. Given the known pro-oxidative effect of NO and the proposed role of oxidative stress in the pathogenesis of RA, this study explores whether SE-triggered signaling can increase cellular oxidative stress. cAMP levels, adenylyl cyclase activity, and protein kinase A activity were measured using commercial kits. Generation of reactive oxygen species (ROS) was quantified using the fluorochrome dichlorofluorescein diacetate. Oxidative DNA damage was quantified using the single-cell electrophoresis technique. Here, we report that cells e…

Arthritis RheumatoidB-LymphocytesOxidative StressAdenosineEpitopes B-LymphocyteHumansDisease SusceptibilityReactive Oxygen SpeciesAntioxidantsSignal TransductionResearch ArticleArthritis researchtherapy
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The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses.

2011

Abstract Lymphnode swelling during immune responses is a transient, finely regulated tissue rearrangement, accomplished with the participation of the extracellular matrix. Here we show that murine and human reactive lymph nodes express SPARC in the germinal centres. Defective follicular dendritic cell networking in SPARC-deficient mice is accompanied by a severe delay in the arrangement of germinal centres and development of humoral autoimmunity, events that are linked to Th17 development. SPARC is required for the optimal and rapid differentiation of Th17 cells, accordingly we show delayed development of experimental autoimmune encephalomyelitis whose pathogenesis involves Th17. Not only h…

Autoimmune diseases; Extracellular matrix; Germinal centre reaction; Th17 cellsEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyCell CommunicationBiologyfollicular dendritic cellExtracellular matrixAnimals Genetically ModifiedMiceImmune systemSPARC; follicular dendritic cell; Th17Autoimmune diseasemedicinegerminal centre reactionImmunology and AllergyAnimalsHumansautoimmune diseasesOsteonectinMice KnockoutB-LymphocytesCD40Follicular dendritic cellsExperimental autoimmune encephalomyelitisMatricellular proteinGerminal centerSPARCCell Differentiationmedicine.diseaseCell biologyExtracellular MatrixImmunity HumoralMice Inbred C57BLCrosstalk (biology)Disease Models AnimalImmunologybiology.proteinDisease ProgressionTh17 CellsImmunizationMyelin-Oligodendrocyte GlycoproteinTh17autoimmune diseases; extracellular matrix; germinal centre reaction; th17 cellsDendritic Cells FollicularMyelin ProteinsJournal of autoimmunity
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Cross-reactivity of a pathogenic autoantibody to a tumor antigen in GABA(A) receptor encephalitis

2021

Encephalitis associated with antibodies against the neuronal gamma-aminobutyric acid A receptor (GABA A -R) is a rare form of autoimmune encephalitis. The pathogenesis is still unknown but autoimmune mechanisms were surmised. Here we identified a strongly expanded B cell clone in the cerebrospinal fluid of a patient with GABA A -R encephalitis. We expressed the antibody produced by it and showed by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry that it recognizes the GABA A -R. Patch-clamp recordings revealed that it tones down inhibitory synaptic transmission and causes increased excitability of hippocampal CA1 pyramidal neurons. Thus, the antibody likely contributed to…

AutoimmunityCross Reactionsmedicine.disease_causeCross-reactivityAutoantigensPathogenesisAutoimmune Diseases of the Nervous SystemAntigens NeoplasmmedicineHumansAutoantibodiesAutoimmune encephalitisB-LymphocytesMultidisciplinarybiologyPyramidal CellsAutoantibodyGABA-A-receptor encephalitis autoantibody autoimmune encephalitis epilepsy paraneoplastic encephalitisBiological Sciencesmedicine.diseaseReceptors GABA-ATumor antigennervous systemImmunologybiology.proteinImmunohistochemistryEncephalitisDisease SusceptibilityAntibodyEncephalitisBiomarkers
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Overexpression of Bcl-3 inhibits the development of marginal zone B cells.

2013

The transcription factor Bcl-3 functions as a proto-oncogene via regulation of cell proliferation and apoptosis. Bcl-3 is an atypical member of the IκB family and plays a central role in the immune response through interactions with the NF-κB subunits p50 and p52. To investigate the impact of Bcl-3 on B-cell maturation and regulation, we generated mice that overexpress Bcl-3 specifically in B cells. Interestingly, these mice lack marginal zone B cells and exhibit a significant reduction in the number of B-1 B cells. Further, B cells from these mice are impaired in their proliferative capacity. Our data demonstrate that the overexpression of the transcription factor Bcl-3 inhibits germinal c…

B-LymphocytesCell growthImmunologyGerminal centerGene ExpressionNF-κBBiologyMarginal zoneGerminal CenterMolecular biologyCell biologychemistry.chemical_compoundMiceImmune systemchemistryApoptosisB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsMarginal zone B-cellImmunology and AllergyAnimalsTranscription factorCell ProliferationTranscription FactorsEuropean journal of immunology
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Interleukin 27 induces differentiation of neural C6-precursor cells into astrocytes.

2007

Interleukin 6 (IL6)-type cytokines are major regulators of inflammation and thereby contribute to the neuropathology and pathophysiology associated with inflammation of the central nervous system (CNS). Furthermore, astrocyte development which is a key process in the development of the CNS is also controlled by cytokines of the IL6-family. Interleukin 27 (IL27) is a recently identified member of this family and has been implicated in the inhibition of TH17 T-cell-responses. Here we show that IL27 and the HHV8 encoded viral IL6 (vIL6) induce C6 glioma cells to differentiate into an astrocyte-like state. Cytokine stimulation led to STAT-factor phosphorylation and consequently to protein expre…

B-LymphocytesInterleukin-6Interleukin-17BiophysicsInterleukinCell DifferentiationCell BiologyBiologyBiochemistryCell biologyCell LineInterleukin 33Astrocyte differentiationInterleukin 32MiceInterleukin 20AstrocytesImmunologyAnimalsInterleukin 27Molecular BiologyInterleukin 4Interleukin 3Biochemical and biophysical research communications
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Cytokines in the pathophysiology and treatment of chronic B-cell malignancies

1995

Chronic B-cell malignancies are characterized by accumulation of transformed B cells of low proliferative index in lymphatic and extralymphatic tissues. Cytokines do not appear to play a role in the primary step of transformation. However, proliferation as well as inhibition of apoptosis of malignant B cells can readily be explained by cytokine effects. Clinical trials of interferons (IFN) and interleukin-2 alone or in combination have been performed in patients with hairy cell leukemia (HCL), CLL, and low- and intermediate-grade non-Hodgkin's lymphoma. While IFN alpha became standard therapy of HCL, responses in other entities were variable, ranging from 0 to 70% in selected populations. C…

B-LymphocytesLeukemia Hairy CellChemotherapyLeukemiabusiness.industryLymphoma Non-Hodgkinmedicine.medical_treatmentChronic lymphocytic leukemiaHematologyGeneral MedicineImmunotherapymedicine.diseaseLeukemia Lymphocytic Chronic B-CellLymphomaLymphatic systemCytokinemedicine.anatomical_structureImmunologymedicineCytokinesHumansHairy cell leukemiabusinessB cellAnnals of Hematology
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Pathogenesis of primary Sjögren's syndrome beyond B lymphocytes

2020

Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder affecting exocrine glands of the body, prevalently lacrimal and salivary glands. The pSS pathogenesis has been thought to be B-cell-centric and several clinical trials have been carried out in order to clarify the therapeutic role of B-cell depletion in patients with pSS. Unfortunately, however, B-cell depletion with rituximab has failed in demonstrating any significant results in pSS patients. Besides the contribution of B cells in the pathogenesis of pSS, effector Tfh, Th17 and Th22 cells, follicular dendritic cells (DCs), innate cells (ICs) and several cytokines, chemokines and miRNA have been proved to participate to the …

B-LymphocytesMicroRNAsstomatognathic diseasesSjogren's Syndromestomatognathic systemB-LymphocyteSjogren's Syndrome.HumansMicroRNARituximabSalivary GlandSalivary GlandsHuman
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Autoimmunity seen through the SEREX-scope.

2003

Autoantibodies can be detected in autoimmune diseases with a long prodromal phase and may serve as early indicators of disease activity. Autoantibody-based screening methods are therefore potent tools for the identification of target antigens. The SEREX method (serological identification of antigens by recombinant expression cloning) has been developed for the serological definition of immunogenic tumor antigens. Recent studies indicate that the SEREX approach may also be utilized for the analysis of complex immune responses involved in autoimmune diseases.

B-LymphocytesRecombinant expressionImmunologyAutoantibodyAutoimmunityBiologymedicine.disease_causeRecombinant ProteinsAutoimmunitySerologyAutoimmune DiseasesMiceImmune systemImmunizationAntigenImmunologyScreening methodmedicineImmunology and AllergyAnimalsHumansImmunizationSerologic TestsAutoantibodiesAutoimmunity reviews
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Invariant NKT cells are expanded in peripheral blood but are undetectable in salivary glands of patients with primary Sjögren's syndrome

2016

OBJECTIVES: Invariant NKT (iNKT) cells play a role in regulating the function of autoreactive B cells before their entry into germinal centres. Absence and/or reduction of iNKT cells have been demonstrated in patients with systemic lupus erythematosus (SLE) together with an increase of autoreactive B cell activity. Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease in which lymphocyte infiltration and organisation in lymphoid structures of inflamed salivary glands occurs. The aim of the study was to investigate the percentage and function of iNKT in the salivary glands and peripheral blood of patients with pSS. METHODS: Minor salivary gland biopsies were obtained from patient…

BiopsyReceptors Antigen T-CellFluorescent Antibody TechniqueEnzyme-Linked Immunosorbent AssayCell CommunicationLymphocyte ActivationReal-Time Polymerase Chain ReactionSalivary GlandsInterferon-gammastomatognathic systemHumansLymphocyte CountCells CulturedCell ProliferationB-LymphocytesInterleukin-17Flow CytometryCoculture TechniquesSettore MED/16 - Reumatologiastomatognathic diseasesIL-17Sjogren's SyndromeAntibodies AntinuclearCase-Control StudiesAntibody FormationNatural Killer T-CellsSjögren's syndromeNKT cellNKT cells Sjögren's syndrome IL-17
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