Search results for " allergy"

showing 10 items of 3043 documents

Circulation and diagnostics of Puumala virus in Norway: nephropatia epidemica incidence and rodent population dynamics.

2017

Hantaviruses pose a public health concern worldwide causing haemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Puumala virus (PUUV) is the most prevalent hantavirus in Central and Northern Europe, and causes a mild form of HFRS, also known as nephropathia epidemica (NE). In nature, the main host of PUUV is the bank vole (Myodes glareolus), and transmission to humans occurs through inhalation of aerosols from rodent excreta. Nephropathia epidemica is particularly prevalent in Nordic countries, however, few studies of PUUV have been performed in Norway. The aim of this study was to analyse the dynamics of PUUV in Norway and compare with bank vole population…

0301 basic medicineMaleSerumRodentanimal diseasesvirusesPopulation DynamicsSequence HomologyPolymerase Chain ReactionPuumala virusImmunology and AllergyMedicineCluster AnalysisHaemorrhagic feverChildPhylogenyAged 80 and overeducation.field_of_studybiologyArvicolinaeNorwayIncidence (epidemiology)Incidencevirus diseasesGeneral MedicineMiddle AgedChild PreschoolHemorrhagic Fever with Renal SyndromePuumala virusFemaleTopography MedicalSeasonsMicrobiology (medical)Adultmedicine.medical_specialtyAdolescent030106 microbiologyPopulationHantavirus Pulmonary SyndromeReal-Time Polymerase Chain ReactionPathology and Forensic Medicine03 medical and health sciencesYoung Adultbiology.animalAnimalsHumanseducationAgedHantavirus pulmonary syndromebusiness.industryPublic healthInfant NewbornInfantSequence Analysis DNAbiology.organism_classificationVirologyrespiratory tract diseases030104 developmental biologybusinessAPMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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Mast cells are associated with the onset and progression of celiac disease

2017

Background Celiac disease (CD) is an immune-mediated disorder characterized by an accumulation of immune cells in the duodenal mucosa as a consequence of both adaptive and innate immune responses to undigested gliadin peptides. Mast cells (MCs) are innate immune cells that are a major source of costimulatory signals and inflammatory mediators in the intestinal mucosa. Although MCs have previously been associated with CD, functional studies have never been performed. Objective We aimed at evaluating the role of MCs in the pathogenesis of CD. Methods Intestinal biopsy specimens of patients with CD were scored according to the Marsh classification and characterized for leukocyte infiltration a…

0301 basic medicineMaleSettore MED/09 - Medicina InternaImmunologygliadin immunologyFluorescent Antibody TechniqueBiologyCell DegranulationGliadinProinflammatory cytokinePathogenesis03 medical and health sciencesMice0302 clinical medicineImmune systemIntestinal mucosamedicineImmunology and AllergyAnimalsHumansCeliac diseaseMast CellsIntestinal Mucosap31-43 fragmentToll-like receptorInnate immune systemCeliac disease; gliadin immunology; mast cell; p31-43 fragment; mast cellFOXP3Mast cellImmunohistochemistryhumanitiesPeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyDisease ProgressionFemalemast cell
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HLA-C1 ligands are associated with increased susceptibility to systemic lupus erythematosus.

2017

Recently, the role of killer cell immunoglobulin-like receptor (KIR) in autoimmune diseases has received increasing attention. The present study was undertaken to determine the association of KIR genes and the human leukocytes antigen (HLA) ligands with Systemic Lupus Erythematosus (SLE) and accompanying oxidative stress. Presence or absence of 17 KIR and 5 HLA loci was performed using the polymerase chain reaction-sequence specific primer (PCR-SSP) method by case-control study. A total of 45 SLE patients, and 60 healthy controls, all of Sicilian descent, were enrolled. Plasma values of the anti-oxidant molecule Taurine were determined in all subjects by capillary electrophoresis UV detecti…

0301 basic medicineMaleTaurineTaurineCellSLEDiseasemedicine.disease_causechemistry.chemical_compound0302 clinical medicineReceptors KIRImmunology and AllergyLupus Erythematosus SystemicReceptorSicilyGeneral MedicineMiddle AgedKIRHLAmedicine.anatomical_structureDisease ProgressionFemaleCase-Control StudieHumanAdultNKImmunologyGenetic Association StudieHuman leukocyte antigenHLA-C Antigens03 medical and health sciencesYoung AdultAntigenmedicineHumansGeneGenetic Association StudiesSettore MED/04 - Patologia Generale030203 arthritis & rheumatologyHLA-C Antigenbusiness.industryOxidative StreSettore MED/16 - ReumatologiaOxidative Stress030104 developmental biologychemistryCase-Control StudiesImmunologybusinessOxidative stressHuman immunology
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Genetic justification of severe COVID-19 using a rigorous algorithm

2021

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (…

0301 basic medicineMaleThrombomodulinSeverity of Illness Index0302 clinical medicineRisk FactorsImmunology and AllergyMedicineComplement ActivationRigorous algorithmmedicine.diagnostic_testHigh-Throughput Nucleotide SequencingComplement C3EculizumabEculizumabMiddle AgedHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsFactor HComplement Factor HFemaleAlgorithmsmedicine.drugmedicine.medical_specialtyThrombotic microangiopathyCritical CareImmunologyComplementADAMTS13 Protein03 medical and health sciencesInternal medicineFull Length ArticleSeverity of illnessGenetic predispositionGenetic susceptibilityHumansGenetic Predisposition to DiseaseGenetic TestingRisk factorGenetic testingAgedbusiness.industryThrombotic MicroangiopathiesCOVID-19medicine.diseaseComplement system030104 developmental biologySARS-CoV2business030215 immunologyClinical Immunology (Orlando, Fla.)
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Brief Report: Functional Interaction of Endoplasmic Reticulum Aminopeptidase 2 and HLA-B27 Activates the Unfolded Protein Response.

2017

Objective: The basic mechanisms underlying the pathogenesis of ankylosing spondylitis (AS) remain unresolved. We previously reported an association of the single-nucleotide polymorphism (SNP) rs2549782 in the endoplasmic reticulum aminopeptidase 2 gene (ERAP2) with AS. It is known that patients homozygous for the G allele (GG) of another ERAP2 SNP, rs2248374, lack expression of ERAP2 (ERAP2 null). The present study utilized this information to study the impact of ERAP2 deficiency on HLA–B27 expression in patients with AS, specifically focusing on the functional interaction of ERAP2 and HLA–B27 in peripheral blood mononuclear cells (PBMCs) from patients with AS and assessing the effects …

0301 basic medicineMaleX-Box Binding Protein 1Aminopeptidases0302 clinical medicineImmunology and AllergyRNA Small InterferingEndoplasmic Reticulum Chaperone BiPHLA-B27 AntigenHeat-Shock ProteinsAlleleBlottingReverse Transcriptase Polymerase Chain ReactionHeat-Shock ProteinSingle NucleotideMiddle AgedFlow CytometryCCAAT-Enhancer-Binding Protein3. Good healthUp-RegulationFemaleWesternHumanAnkylosingAdultAminopeptidaseMononuclearImmunologyBlotting WesternSingle-nucleotide polymorphismBiologyMajor histocompatibility complexSmall InterferingPolymorphism Single NucleotideAdult; Alleles; Aminopeptidases; Blotting Western; CCAAT-Enhancer-Binding Proteins; Cell Line; Female; Flow Cytometry; HLA-B27 Antigen; Heat-Shock Proteins; Humans; Leukocytes Mononuclear; Male; Middle Aged; Polymorphism Single Nucleotide; RNA Small Interfering; Reverse Transcriptase Polymerase Chain Reaction; Spondylitis Ankylosing; Unfolded Protein Response; Up-Regulation; X-Box Binding Protein 1; Immunology and Allergy; Rheumatology; ImmunologyCell Line03 medical and health sciencesDownregulation and upregulationRheumatologyHumansSpondylitis AnkylosingAllelePolymorphismAlleles030203 arthritis & rheumatologySpondylitiHLA-B27LeukocyteEndoplasmic reticulum aminopeptidase 2X-Box Binding Protein 1Molecular biologySettore MED/16 - Reumatologia030104 developmental biologyUnfolded protein responsebiology.proteinCCAAT-Enhancer-Binding ProteinsLeukocytes MononuclearUnfolded Protein ResponseRNAArthritisrheumatology (Hoboken, N.J.)
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Analysis of colon-infiltrating γδ T cells in chronic inflammatory bowel disease and in colitis-associated cancer

2019

Abstract Inflammatory bowel disease (IBD) remains a global health problem with a significant percentage of patients progressing to chronic inflammation and colitis-associated cancer (CAC). Whether or not γδ T cells contribute to initiation and maintenance of inflammation in IBD and in the development of CAC is not known. We have evaluated the frequency, phenotype, and functions of γδ T cells among tissue-infiltrating lymphocytes in healthy donors and IBD and CAC patients. Results show that Vδ1 T cells are the dominant γδ T-cell population in healthy tissue, whereas Vδ2 T significantly abound in chronic IBD. Vδ2 T cells produce more IFN-γ, TNF-α, and IL-17 than Vδ1 T cells in chronic inflame…

0301 basic medicineMalechronic inflammationγδ T&nbspmedicine.medical_treatmentInflammatory bowel diseasePathogenesis0302 clinical medicineT-Lymphocyte SubsetsImmunology and AllergyCACeducation.field_of_studyReceptors Antigen T-Cell gamma-deltaMiddle AgedColitisIL-17Cytokine030220 oncology & carcinogenesisColonic NeoplasmsCytokinesFemaleInterleukin 17Disease Susceptibilitymedicine.symptomAdultImmunologyPopulationIBDInflammationBiologyProinflammatory cytokineImmunophenotyping03 medical and health sciencesmedicineHumansLymphocyte CountColitiseducationAgedGene Expression ProfilingCell Biologymedicine.diseaseInflammatory Bowel Diseasesdigestive system diseases030104 developmental biologycolitiImmunologyChronic DiseasecellsBiomarkers
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Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibrobla…

2018

Abstract Background Fibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process. Methods After ethical approval was obtained, skin biopsies were co…

0301 basic medicineMalelcsh:Diseases of the musculoskeletal systemProton Pump InhibitorFibrosiCellular differentiationmedicine.medical_treatmentSystemic sclerosiFibrosisImmunology and AllergyMedicineMyofibroblastsskin and connective tissue diseasesCells CulturedSkinintegumentary systemCell DifferentiationMiddle AgedMesenchymal Stem CellBenzamidesSystemic sclerosisFemaleMyofibroblastResearch ArticleHumanAdultStromal cellImmunology03 medical and health sciencesYoung AdultRheumatologyBenzamideAntigens CDAntigens NeoplasmHumansGene silencingCell ProliferationMyofibroblastScleroderma Systemicbusiness.industryGrowth factorMesenchymal stem cellStromal CellMesenchymal Stem CellsProton Pump Inhibitorsmedicine.diseaseFibrosisCD248Settore MED/16 - Reumatologia030104 developmental biologyCancer researchStromal Cellslcsh:RC925-935CD248; Fibrosis; Systemic sclerosis; Rheumatology; Immunology and Allergy; ImmunologybusinessTransforming growth factor
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CD3ε Expression Defines Functionally Distinct Subsets of Vδ1 T Cells in Patients With Human Immunodeficiency Virus Infection

2018

Human γδ T cells expressing the Vδ1 T cell receptor (TCR) recognize self and microbial antigens and stress-inducible molecules in a major histocompatibility complex -unrestricted manner and are an important source of innate interleukin-17. Vδ1 T cells are expanded in the circulation and intestines of patients with human immunodeficiency virus (HIV) infection. In the present study, we show that patients with HIV have elevated frequencies, but not absolute numbers, of circulating Vδ1 T cells compared to control subjects. This increase was most striking in the patients with Candida albicans co-infection. Using flow cytometry and confocal microscopy, we identify two populations of Vδ1 T cells, …

0301 basic medicineMalelcsh:Immunologic diseases. AllergyCD3 ComplexCD3T cellVδ1 T cellsImmunologyGene ExpressionHIV InfectionsMajor histocompatibility complexFlow cytometryImmunophenotypinginterleukin-1703 medical and health sciencesImmunophenotypingAntigenT-Lymphocyte SubsetsmedicineHumansImmunology and AllergyLymphocyte CountOriginal Researchprogrammed death-1biologymedicine.diagnostic_testhuman immunodeficiency virusCoinfectionflow cytometryT-cell receptorCandidiasisReceptors Antigen T-Cell gamma-deltaMolecular biology030104 developmental biologymedicine.anatomical_structurebiology.proteinHIV-1CytokinesFemaleInterleukin 17lcsh:RC581-607CD3εBiomarkersFrontiers in Immunology
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Retrospective Analysis of Checkpoint Inhibitor Therapy-Associated Cases of Bullous Pemphigoid From Six German Dermatology Centers

2021

Immune-related adverse events (irAEs) are a class-effect of checkpoint inhibitors (CIs). The development of a Bullous pemphigoid (BP)-like blistering disease, driven by autoantibodies against the hemidesmosomal protein BP180, is a potentially serious irAE whose incidence seems to be increasing. We therefore set out to characterize the clinical and (immuno)histopathological features and treatment responses of cases of BP which developed during or after CI therapy collated in six German tertiary referral centers between 2014 and 2018. We identified twelve cases of BP which emerged during and/or after CI therapy. The time interval between the initiation of CI therapy and the diagnosis of BP wa…

0301 basic medicineMalelcsh:Immunologic diseases. Allergymedicine.medical_specialtyPD-1 - PD-L1 axisautoantibodiesImmune checkpoint inhibitorsImmunologypemphigoid diseaseIpilimumabPembrolizumabDermatology030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineAntineoplastic Agents ImmunologicalAdrenal Cortex HormonesInternal medicineGermanyNeoplasmsPemphigoid BullousmedicineHumansImmunology and AllergyipilimumabAdverse effectImmune Checkpoint InhibitorsAgedRetrospective StudiesOriginal ResearchAged 80 and overnivolumabbusiness.industryIncidence (epidemiology)autoimmunityAutoantibodyMiddle Agedmedicine.disease030104 developmental biologyFemaleBullous pemphigoidpembrolizumabNivolumabbusinesslcsh:RC581-607checkpoint inhibitorsmedicine.drugFrontiers in Immunology
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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