Search results for "IMM"

showing 10 items of 18201 documents

Cryptosporidiosis Outbreak in Immunocompetent Children from a Remote Area of French Guiana: CRYPTOSPORIDIOSIS OUTBREAK IN AMAZONIAN CHILDREN

2018

International audience; In September 2014, an increase in the number of Cryptosporidium spp. gastrointestinal tract infections was reported over a 6-month period among children living in a remote area along the Maroni River in French Guiana. Children presented gastroenteritis symptoms with Cryptosporidium-positive stools. Questionnaires were administered and stool examinations were controlled 3 months after the onset of symptoms. Data collection included demographics, food consumption, river behavior, symptoms, and outcome. Stool specimens were tested using microscopy and polymerase chain reaction. Samples from the water systems were examined for turbidity and culture for bacteria. Data fro…

0301 basic medicineMaleRural PopulationPediatricsmedicine.medical_specialty030106 microbiologyCryptosporidiosisCryptosporidiumDisease clusterPolymerase Chain ReactionDisease Outbreaks03 medical and health sciencesFeces0302 clinical medicineRiversVirologySurveys and QuestionnairesEpidemiologyMedicineHumans030212 general & internal medicineTypingDemographybiologybusiness.industryIncidence (epidemiology)OutbreakRemote areaInfantCryptosporidium[ SDV.SPEE ] Life Sciences [q-bio]/Santé publique et épidémiologieArticlesbiology.organism_classification3. Good healthFrench GuianaGastroenteritisGastrointestinal TractInfectious DiseasesChild PreschoolParasitology[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieFemalebusinessCryptosporidium hominisImmunocompetence
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Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
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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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Hepatitis E virus-induced primary cutaneous CD30(+) T cell lymphoproliferative disorder.

2017

International audience; BACKGROUND & AIM:Several types of unexplained extra-hepatic manifestations, including haematological disorders, have been reported in the context of hepatitis E virus (HEV) infection. However, the underlying mechanism(s) of these manifestations are unknown. We provide evidence that HEV has an extra-hepatic endothelial tropism that can engage cutaneous T cells towards clonality.METHODS:A patient with a CD30(+) cutaneous T cell lymphoproliferative disorder (T-LPD) and biopsy-proven chronic HEV infection received three rounds of oral ribavirin treatment, administered either without or with interferon, and eventually achieved a sustained virologic response (SVR). Patholo…

0301 basic medicineMaleSkin NeoplasmsLymphomaLymphomatoid papulosisT cellLymphoproliferative disordersKi-1 Antigen[SDV.CAN]Life Sciences [q-bio]/CancerExtra-hepatic manifestationNHL[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciencesInterleukin 210302 clinical medicineEndothelial cellInterferonHepatitis E virusMedicineHumansCD30-positive cutaneous T cell lymphoproliferative disorderTropismHepatologybusiness.industryvirus diseasesMiddle Agedmedicine.diseaseVirologyHepatitis ELymphoma T-Cell CutaneousViral Tropism030104 developmental biologymedicine.anatomical_structureHEVImmunologyTissue tropism030211 gastroenterology & hepatologybusinessMemory T cellCD8medicine.drugJournal of hepatology
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Direct-acting antivirals and visceral leishmaniasis: a case report

2019

Abstract Background Visceral leishmaniasis is a vector-borne parasitic disease caused by protozoa belonging to the genus Leishmania. The clinical presentation of visceral leishmaniasis strictly depends on the host immunocompetency, whereas depressive conditions of the immune system impair the capability to resolve the infection and allow reactivation from sites of latency of the parasite. Case presentation We describe a case of visceral leishmaniasis (VL) that occurred in a patient with chronic hepatitis C treated with direct-acting antiviral drugs (DAA). The hypothesized mechanism is the alteration of protective inflammation mechanisms secondary to DAA therapy. Downregulation of type II an…

0301 basic medicineMaleSofosbuvir030106 microbiologyAntiprotozoal AgentsCase ReportDirect-acting antiviralAntiviral Agentslcsh:Infectious and parasitic diseases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemAmphotericin BRibavirinHumansMedicinelcsh:RC109-216030212 general & internal medicineLeishmania infantumAgedAntiviral AgentLeishmaniaVisceral Leishmaniasisbiologybusiness.industryCoinfectionRibavirinHepatitis CHepatitis C Chronicbiology.organism_classificationmedicine.diseaseLeishmaniaHepatitis CInfectious DiseasesVisceral leishmaniasischemistryAntiprotozoal AgentImmunologyCoinfectionVisceral LeishmaniasiLeishmaniasis VisceralLeishmania infantumSofosbuvirbusinessmedicine.drugHumanBMC Infectious Diseases
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Vitellogenin-like A–associated shifts in social cue responsiveness regulate behavioral task specialization in an ant

2018

Division of labor and task specialization explain the success of human and insect societies. Social insect colonies are characterized by division of labor, with workers specializing in brood care early and foraging later in life. Theory posits that this task switching requires shifts in responsiveness to task-related cues, yet experimental evidence is weak. Here, we show that a Vitellogenin (Vg) ortholog identified in an RNAseq study on the ant T. longispinosus is involved in this process: using phylogenetic analyses of Vg and Vg-like genes, we firstly show that this candidate gene does not cluster with the intensively studied honey bee Vg but falls into a separate Vg-like A cluster. Second…

0301 basic medicineMaleTask switchingAgingFat BodySocial SciencesGene ExpressionGenes InsectBiochemistryFatsVitellogeninsSociologyGene Regulatory NetworksForagingBiology (General)reproductive and urinary physiologyPhylogenyAnimal BehaviorBehavior AnimalGeneral NeuroscienceEukaryotaBeesLipidsANTInsectsAnimal SocialityGene Knockdown TechniquesMultigene FamilySocial SystemsInsect ProteinsFemaleCuesGeneral Agricultural and Biological SciencesHoney BeesDivision of labourResearch ArticleArthropodaQH301-705.5ForagingBiologyModels BiologicalGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesSpecies Specificityddc:570Specialization (functional)GeneticsAnimalsSocial BehaviorBehaviorGeneral Immunology and MicrobiologyAntsfungiOrganismsBiology and Life SciencesHoney beeSocial cueInvertebratesHymenopteraBrood030104 developmental biologyEvolutionary biologyZoologyPLoS Biology
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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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Retinoblastoma Is Characterized by a Cold, CD8+ Cell Poor, PD-L1- Microenvironment, Which Turns Into Hot, CD8+ Cell Rich, PD-L1+ After Chemotherapy.

2021

Purpose To investigate the impact of chemotherapy (CHT) on human retinoblastoma (RB) tumor microenvironment (TME). Cases and Methods Ninety-four RBs were studied, including 44 primary RBs treated by upfront surgery (Group 1) and 50 primary RBs enucleated after CHT (CHT), either intra-arterial (IAC; Group 2, 33 cases) or systemic (S-CHT; Group 3, 17 cases). Conventional and multiplexed immunohistochemistry were performed to make quantitative comparisons among the three groups, for the following parameters: tumor-infiltrating inflammatory cells (TI-ICs); programmed cell death protein 1 (PD-1) positive TI-ICs; Ki67 proliferation index; gliosis; PD-1 ligand (PD-L1) protein expression; vessel nu…

0301 basic medicineMaleTime FactorsProliferation indexRetinal NeoplasmsProgrammed Cell Death 1 Receptorretinoblastoma; tumor microenvironment; chemotherapy; PD-1/PD-L1; multiplexed immunohistochemistry; B7-H1 Antigen; CD8-Positive T-Lymphocytes; Child Preschool; Female; Follow-Up Studies; Humans; Immunohistochemistry; Infant; Infant Newborn; Lymphocytes Tumor-Infiltrating; Male; Programmed Cell Death 1 Receptor; Retinal Neoplasms; Retinoblastoma; Retrospective Studies; Time Factors; Tumor MicroenvironmentCD8-Positive T-LymphocyteschemotherapyPD-1/PD-L1B7-H1 AntigenRetina03 medical and health sciencesretinoblastoma; tumor microenvironment chemotherapy PD-1/PD-L1 multiplexed immunohistochemistry0302 clinical medicineLymphocytes Tumor-InfiltratingPD-L1medicineTumor MicroenvironmentHumansLymphocytesTumor-InfiltratingChildPreschoolAnaplasiaRetrospective StudiesTumor microenvironmentbiologyRetinoblastomaChemistryInfant NewbornRetinoblastomaInfantGeneral Medicinemultiplexed immunohistochemistrymedicine.diseaseNewbornChemotherapy regimenImmunohistochemistry030104 developmental biologyGliosis030220 oncology & carcinogenesisChild Preschoolbiology.proteinCancer researchFemalemedicine.symptomCD8Follow-Up StudiesInvestigative ophthalmologyvisual science
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