Search results for "Unity"

showing 10 items of 3852 documents

B cell activating factor (BAFF): Structure, functions, autoimmunity and clinical implications in Systemic Lupus Erythematosus (SLE)

2020

The B cell activating factor (BAFF), or B lymphocyte stimulator (BLyS), is a B cell survival factor which supports autoreactive B cells and prevents their deletion. BAFF expression is closely linked with autoimmunity and is enhanced by genetic alterations and viral infections. Furthermore, BAFF seems to be involved in adipogenesis, atherosclerosis, neuro-inflammatory processes and ischemia reperfusion (I/R) injury. BAFF is commonly overexpressed in Systemic Lupus Erythematosus (SLE) and strongly involved in the pathogenesis of the disease. The relationship between BAFF levels, disease activity and damage accrual in SLE is controversial, but growing evidence is emerging on its role in renal …

ImmunologyAutoimmunitymedicine.disease_causeAutoimmunityPathogenesisImmune systemstomatognathic systemimmune system diseaseshemic and lymphatic diseasesB-Cell Activating FactormedicineHumansLupus Erythematosus SystemicImmunology and Allergyskin and connective tissue diseasesB-cell activating factorB cellB-LymphocytesSystemic lupus erythematosusbusiness.industrymedicine.diseaseBelimumabstomatognathic diseasesmedicine.anatomical_structureVirus DiseasesImmunologyRituximabbusinessmedicine.drugAutoimmunity Reviews
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A20 deficiency in B cells enhances B-cell proliferation and results in the development of autoantibodies.

2011

A20/TNFAIP3 is an ubiquitin-editing enzyme, important for the regulation of the NF-κB pathway. Mutations in the TNFAIP3 gene have been linked to different human autoimmune disorders. In human B-cell lymphomas, the inactivation of A20 results in constitutive NF-κB activation. Recent studies demonstrate that in mice the germline inactivation of A20 leads to early lethality, due to inflammation in multiple organs of the body. In this report, we describe a new mouse strain allowing for the tissue-specific deletion of A20. We show that B-cell-specific deletion of A20 results in a dramatic reduction in marginal zone B cells. Furthermore, A20-deficient B cells display a hyperactive phenotype repre…

ImmunologyB-Lymphocyte SubsetsInflammationBiologymedicine.disease_causeLymphocyte ActivationGermlineAutoimmunityMiceimmune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyAnimalsHumansTumor Necrosis Factor alpha-Induced Protein 3AutoantibodiesCell ProliferationMice KnockoutB-LymphocytesCell growthAutoantibodyIntracellular Signaling Peptides and ProteinsNF-kappa BMarginal zoneGerminal CenterMolecular biologyPhenotypeCell biologyCysteine EndopeptidasesModels Animalbiology.proteinmedicine.symptomAntibodySignal TransductionEuropean journal of immunology
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Translocation of the nuclear autoantigen La to cell surface: assembly and disassembly with the extracellular matrix.

1991

La (SS-B) protein is known as one major antigenic target for autoantibodies from patients with certain autoimmune diseases such as Sjogren's syndrome or Lupus Erythematosus. La protein belongs to the so called "extractable nuclear antigens". Here we report that La antigen is not restricted to the nucleus as one might deduce from the exclusive nuclear staining pattern of patient anti-La antibodies but after stimulation of serum-starved cells with 10% fetal calf serum (FCS) appears and stays for at least 45 min at the outer surface of CV-1 cells being available for binding of anti-La antibodies. In addition we found that a minor part of La antigen associates with the extracellular fibronectin…

ImmunologyBiological Transport ActiveAutoimmunityBiologyIn Vitro TechniquesAutoantigensEpitopeExtracellular matrixEpitopesAntigenExtracellularImmunology and AllergyHumansNuclear proteinCells CulturedCell NucleusInflammationCell MembraneMolecular biologyExtracellular MatrixFibronectinBiochemistryMicroscopy FluorescenceRibonucleoproteinsCell cultureMercuric Chloridebiology.proteinElectrophoresis Polyacrylamide GelAntibodyAutoimmunity
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MicroRNAs play a central role in molecular dysfunctions linking inflammation with cancer.

2013

It is now largely admitted that a pro-inflammatory environment may curtail anti-tumor immunity and favor cancer initiation and progression. The discovery that small non-coding regulatory RNAs, namely microRNAs (miRNAs), regulate all aspects of cell proliferation, differentiation, and function has shed a new light on regulatory mechanisms linking inflammation and cancer. Thus, miRNAs such as miR-21, miR-125b, miR-155, miR-196, and miR-210 that are critical for the immune response or hypoxia are often overexpressed in cancers and leukemias. Given the high number of their target transcripts, their deregulation may have a number of deleterious consequences, depending on the cellular context. In…

ImmunologyBiologyBioinformaticsmedicine.disease_causemiR-155Transforming Growth Factor betaNeoplasmsmicroRNAmedicineImmunology and AllergyAnimalsHumansTranscription factorCell ProliferationRegulation of gene expressionInflammationImmunityBiological TherapyGene Expression Regulation NeoplasticMicroRNAsCell Transformation NeoplasticTumor EscapeCancer researchTumor EscapeSignal transductionCarcinogenesisTransforming growth factorSignal TransductionTranscription FactorsImmunological reviews
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Enrichment of Immediate-Early 1 (m123/pp89) Peptide-Specific CD8 T Cells in a Pulmonary CD62LloMemory-Effector Cell Pool during Latent Murine Cytomeg…

2000

ABSTRACTInterstitial cytomegalovirus (CMV) pneumonia is a clinically relevant complication in recipients of bone marrow transplantation (BMT). Recent data for a model of experimental syngeneic BMT and concomitant infection of BALB/c mice with murine CMV (mCMV) have documented the persistence of tissue-resident CD8 T cells after clearance of productive infection of the lungs (J. Podlech, R. Holtappels, M.-F. Pahl-Seibert, H.-P. Steffens, and M. J. Reddehase, J. Virol. 74:7496–7507, 2000). It was proposed that these cells represent antiviral “standby” memory cells whose functional role might be to help prevent reactivation of latent virus. The pool of pulmonary CD8 T cells was composed of two…

ImmunologyCytomegalovirusPeptideCD8-Positive T-LymphocytesBiologyEffector cellMicrobiologyImmediate-Early ProteinsMiceInterleukin 21Latent VirusAntigenVirologyAnimalsCytotoxic T cellAntigens ViralLungAntigenic peptidechemistry.chemical_classificationMice Inbred BALB Cvirus diseasesVirologyVirus LatencyCytomegalovirus infectionchemistryInsect ScienceCytomegalovirus InfectionsImmunologyPathogenesis and ImmunityFemaleImmunologic MemoryJournal of Virology
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Nucleic acid recognizing Toll-like receptors and autoimmunity

2007

The understanding of autoimmune diseases experienced an impressive boost since the Toll-like receptors (TLRs) have been identified as possible key players in autoimmune pathophysiology. Although these receptors recognize a variety of structures derived from viruses, bacteria, and fungi leading to subsequent initiation of the relevant immune responses, recent data support the idea that TLRs are crucial in the induction and perpetuation of certain autoimmune diseases, especially the systemic lupus erythematosus (SLE). In this review, we will summarize recent data on involvement of TLRs in the development of autoimmune diseases. We will focus on TLRs 7, 8, and 9 that were originally identified…

ImmunologyGene ExpressionReceptors Antigen B-CellAutoimmunityContext (language use)Biologymedicine.disease_causeAutoimmune DiseasesAutoimmunityImmune systemAntigenGene expressionmedicineAnimalsHumansImmunology and AllergyReceptorToll-Like ReceptorsRNADNADendritic CellsToll-Like Receptor 7Toll-Like Receptor 8Toll-Like Receptor 9ImmunologyRNASignal transductionSignal TransductionCurrent Opinion in Immunology
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Altered metabolism of gut microbiota contributes to chronic immune activation in HIV-infected individuals.

2015

Altered interplay between gut mucosa and microbiota during treated HIV infection may possibly contribute to increased bacterial translocation and chronic immune activation, both of which are predictors of morbidity and mortality. Although a dysbiotic gut microbiota has recently been reported in HIV + individuals, the metagenome gene pool associated with HIV infection remains unknown. The aim of this study is to characterize the functional gene content of gut microbiota in HIV + patients and to define the metabolic pathways of this bacterial community, which is potentially associated with immune dysfunction. We determined systemic markers of innate and adaptive immunity in a cohort of HIV-in…

ImmunologyHIV InfectionsBiologyGut floraAdaptive ImmunityMicrobiologyMetabolomicsImmunityAntiretroviral Therapy Highly ActiveRNA Ribosomal 16SMetabolomeImmunology and AllergyCluster AnalysisHumansMetabolomicsGeneCase-control studyBayes TheoremBiodiversityAcquired immune systembiology.organism_classificationImmunity InnateMarkov ChainsGastrointestinal MicrobiomeMetabolic pathwayCase-Control StudiesImmunologyDisease ProgressionHIV-1MetabolomeMetagenomeMucosal immunology
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Mast cells are crucial for early inflammation, migration of Langerhans cells, and CTL responses following topical application of TLR7 ligand in mice.

2007

Abstract Until recently, IgE-activated mast cells have been regarded merely as effector cells of adaptive immune responses, involved in allergic reactions and mucosal immunity to parasites. Herein, we report that murine dermal mast cells, activated by local administration of a cream containing the synthetic TLR7 ligand imiquimod, are essential to initiate an early inflammatory reaction. The mast-cell–derived cytokines TNF-α and IL-1β play an important role in this process. Furthermore, TLR7-activated mast cells are also able to promote the emigration of Langerhans cells, which partly depends on the expression of mast-cell–derived IL-1β. We have previously shown that TLR7 ligation enhances t…

ImmunologyInterleukin-1betaInflammationImmunoglobulin ELigandsBiochemistryMiceImmune systemAdjuvants ImmunologicCell MovementmedicineCytotoxic T cellAnimalsMast CellsAntigensSkinInflammationImmunity CellularMice Inbred BALB CVaccinesImiquimodMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaDegranulationCell BiologyHematologyTLR7Immunoglobulin EAcquired immune systemImmunity InnateInterleukin 33Toll-Like Receptor 7Langerhans CellsImmunologybiology.proteinAminoquinolinesImmunizationmedicine.symptomAgranulocytosisT-Lymphocytes CytotoxicBlood
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Functional C1-inhibitor diagnostics in hereditary angioedema: Assay evaluation and recommendations

2008

Hereditary angioedema (HAE) is an autosomal dominant disease characterized by recurrent episodes of potentially life-threatening angioedema. The most widespread underlying genetic deficiency is a heterozygous deficiency of the serine protease inhibitor Cl esterase inhibitor (C1-Inh). In addition to low C4 levels, the most important laboratory parameter for correct diagnosis of HAE or angioedema due to acquired C1-Inh deficiency is reduced C1-Inh function (fC1-Inh). No direct recommendations about the assays for fC1-Inh or sample handling conditions are available, although this would prove especially useful when a laboratory first starts to offer assays on fC1-Inh for HAE diagnosis. In the p…

ImmunologyMESH: Complement C1 Inactivator ProteinsEnzyme-Linked Immunosorbent AssayMESH: Blood Specimen CollectionComplement C1 Inactivator Proteins[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityC1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansImmunology and AllergyMESH: Angioedemaheterocyclic compoundsAngioedema030304 developmental biologySample handlingBlood Specimen Collection0303 health sciencesMESH: HumansAngioedemabiologybusiness.industryTemperatureAutosomal dominant traitMESH: Enzyme-Linked Immunosorbent Assaybiochemical phenomena metabolism and nutritionrespiratory system[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismSerum samplesmedicine.diseasebacterial infections and mycosesMESH: Temperature3. Good healthC1 esteraserespiratory tract diseases030228 respiratory systemImmunologyHereditary angioedemabiology.proteinmedicine.symptombusinessJournal of Immunological Methods
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Mast Cells Are Key Promoters of Contact Allergy that Mediate the Adjuvant Effects of Haptens

2011

SummaryA prominent feature of sensitizing environmental compounds that cause allergic contact dermatitis is the rapid induction of an innate inflammatory response that seems to provide danger signals for efficient T cell priming. We generated mouse models of mast cell deficiency, mast cell-specific gene inactivation, and mast cell reporter mice for intravital imaging and showed that these adjuvant effects of contact allergens are mediated by mast cells and histamine. Mast cell deficiency resulted in impaired emigration of skin DCs to the lymph node and contact hypersensitivity was dramatically reduced in the absence of mast cells. In addition, mast cell-specific inactivation of the Il10 gen…

ImmunologyMedizinPriming (immunology)BiologyMicechemistry.chemical_compoundImmune systemAdjuvants ImmunologicCell MovementmedicineAnimalsImmunology and AllergyMast CellsInterleukin 5Allergic contact dermatitisNeovascularization PathologicDendritic CellsHypertrophymedicine.diseaseMast cellImmunity InnateMice Inbred C57BLInterleukin 33Interleukin 10medicine.anatomical_structureInfectious DiseaseschemistryDermatitis Allergic ContactMutationImmunologyLymph NodesHaptensHistamineHistamineImmunity
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