Search results for "Immunity"

showing 10 items of 1537 documents

Immunological characteristics of non-intensive care hospitalized COVID-19 patients: A preliminary report

2021

The outbreak of coronavirus disease 2019 (COVID-19) is posing a threat to global health. This disease has different clinical manifestations and different outcomes. The immune response to the novel 2019 coronavirus is complex and involves both innate and adaptive immunity. In this context, cell-mediated immunity plays a vital role in effective immunity against SARS-CoV-2. Significant differences have been observed when comparing severe and non-severe patients. Since these immunological characteristics have not been fully elucidated, we aimed to use cluster analysis to investigate the immune cell patterns in patients with COVID-19 who required hospitalization but not intensive care. We identi…

Lymphocytelcsh:MedicineArticleimmune system deficiency03 medical and health sciences0302 clinical medicineImmune systemImmunityIntensive caremedicineCytotoxic T cell030304 developmental biology0303 health sciencesbiologybusiness.industrySARS-CoV-2lcsh:RGeneral MedicineAcquired immune systemmedicine.anatomical_structureGranzymemultiparametric flow cytometryImmunologybiology.proteinbusinessCluster analysis Immune system deficiencyMultiparametric flow cytometry SARS-CoV-2CD8030215 immunologycluster analysis
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Associations of non-Hodgkin Lymphoma (NHL) risk with autoimmune conditions according to putative NHL loci.

2015

Autoimmune conditions and immune system-related genetic variations are associated with risk of non-Hodgkin lymphoma (NHL). In a pooled analysis of 8,692 NHL cases and 9,260 controls from 14 studies (1988-2007) within the International Lymphoma Epidemiology Consortium, we evaluated the interaction between immune system genetic variants and autoimmune conditions in NHL risk. We evaluated the immunity-related single nucleotide polymorphisms rs1800629 (tumor necrosis factor gene (TNF) G308A), rs1800890 (interleukin-10 gene (IL10) T3575A), rs6457327 (human leukocyte antigen gene (HLA) class I), rs10484561 (HLA class II), and rs2647012 (HLA class II)) and categorized autoimmune conditions as prim…

LymphomaEpidemiologyOriginal Contributionstumor necrosis factorFollicular lymphomaNon-HodgkininteractionSingle-nucleotide polymorphismHuman leukocyte antigenmedicine.disease_causePolymorphism Single NucleotideAutoimmune DiseaseMedical and Health SciencesMathematical SciencesAutoimmunityAutoimmune DiseasesRare Diseasesimmune system diseasesHLA Antigenshuman leukocyte antigenhemic and lymphatic diseasesGenotypemedicineGeneticsHumans2.1 Biological and endogenous factorsPolymorphismAetiologyCancerbusiness.industryTumor Necrosis Factor-alphaLymphoma Non-HodgkinInflammatory and immune systemautoimmune conditionsOdds ratioSingle NucleotideHematologymedicine.diseaseAutoimmune conditions - risk of non-Hodgkin lymphoma (NHL)LymphomaInterleukin-10Case-Control StudiesImmunologyHIV/AIDSbusinessDiffuse large B-cell lymphomaenvironment
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Study of the stress-related signalling of endoplasmic reticulum in grapevine immunity associated to LysM receptor kinases (VvLYKs)

2023

In the actual situation of decreasing the use of chemicals in agriculture, enhancing our understanding of plant immunity is a critical task to develop more sustainable plant health protection methods. An interesting strategy is to study how plants, and in particular grapevine, perceives and responds to different microorganisms. Microorganisms are notably recognizedby LysM Receptor-like Kinase (LYKs) and previous works have identified 16 LYKs encoded by the grapevine genome (VvLYKs) (Roudaire et al. 2023). Among them, VvLYK1-1, VvLYK1-2 and VvLYK5-1 are involved in chitin perception and thus play a role in the plant immunity. Interestingly, immune responses are also involved during symbiotic…

LysM receptor like kinase[SDV] Life Sciences [q-bio]Unfolded Protein ResponseMyc-factorsPlant ImmunityEndoplasmic Reticulum
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Phenoloxidases in ascidian hemocytes: characterization of the pro-phenoloxidase activating system.

2003

The phenoloxidase (PO) activity of the hemocytes lysate supernatant from three ascidians species, assayed by means of 3-methyl-2-benzothiazolinone hydrazone hydrochloride, have been compared. PO-containing hemocytes were identified by a cytochemical reaction and the enzymatic activity measured by a spectrophotometric assay of lysate supernatant from hemocyte populations separated on a discontinuous Percoll density gradient. In Styela plicata, the enzyme appeared to be contained in morula cells only. In Ciona intestinalis, PO activity was shown in univacuolar refractile granulocyte and granular hemocyte. In Phallusia mammillata both compartment cell and granular hemocytes were positive. Enzy…

LysisHemocytesCiona intestinaliCell separationPhysiologySettore BIO/05 - ZoologiaHemocyteBiologyTunicateBiochemistryEnzyme activatormedicineAnimalsCiona intestinalisPhallusia mammillataBenzothiazolesUrochordataMolecular BiologyPolyacrylamide gel electrophoresischemistry.chemical_classificationMonophenol MonooxygenaseImmunityHydrazonesTrypsinbiology.organism_classificationMolecular biologyEnzyme ActivationThiazolesEnzymeStyela plicatachemistryStyela plicataPhenoloxidasePercollmedicine.drugComparative biochemistry and physiology. Part B, Biochemistrymolecular biology
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Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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Research in practice: The impact of interferon-α therapy on immune tolerance

2014

Interferon-α (IFN-α) is the only drug approved for adjuvant therapy of malignant melanoma and is also used in the treatment of hematological and solid tumors. Along with its proven clinical efficacy, IFN-α produces several side effects, particularly with regard to autoimmune disorders. Curious about symptoms of autoimmunity during IFN-α therapy, we asked whether IFN-α directly impacts on immune tolerance. We found that IFN-α does alter the function of tolerogenic dendritic cells (DC) as well as of induced and naturally occurring T-regulatory cells (nTregs). IFN-α blocks the tolerogenic phenotype of DC by inducing maturation and thus preventing the induction of inducible Tregs by DC. It also…

MAPK/ERK pathwayEffectorbusiness.industryMelanomaPhosphodiesteraseDermatologymedicine.disease_causemedicine.diseasePhenotypeAutoimmunityImmune toleranceImmunologymedicineAdjuvant therapybusinessJDDG: Journal der Deutschen Dermatologischen Gesellschaft
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Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.

2008

Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. The main goal of this study was to explore the effects of cigarette smoke extracts (CSE) on Toll-like receptor (TLR) expression and activation in a human bronchial epithelial cell line (16-HBE). The CSE increased the expression of TLR4 and the lipopolysaccharide (LPS) binding, the nuclear factor-kappaB (NF-kappaB) activation, the release of interleukin-8 (IL-8) and the chemotactic activity toward neutrophils. It did not induce TLR2 expression or extracellular signal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increased the expression of TLR4 and induced bot…

MAPK/ERK pathwayLipopolysaccharidesLipopolysaccharideNeutrophilsImmunologyBronchiRespiratory Mucosachemistry.chemical_compoundSmokeTobaccoImmunology and AllergyHumansImmunity MucosalCell Line TransformedMitogen-Activated Protein Kinase 1Toll-like receptorMitogen-Activated Protein Kinase 3Interleukin-8NF-kappa BChemotaxisEpithelial CellsOriginal ArticlesCell biologyChemokine CXCL10Toll-Like Receptor 4TLR2Chemotaxis LeukocytechemistryImmunologyTLR4Respiratory epitheliumSignal transductionSignal TransductionImmunology
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p42 MAPK phosphorylates 80 kDa MARCKS at Ser-113.

1996

Abstract It is demonstrated here that p42 MAPKinase (p42 MAPK) phosphorylates the M yristoylated A lanine- R ich C - K inase S ubstrate (MARCKS) at Ser-113. In permeabilised Swiss 3T3 cells activation of protein kinase C (PKC) leads to p42 MAPK activation, but only the protein kinase C sites in MARCKS become phosphorylated and not Ser-113. The mitogen platelet-derived growth factor (PDGF) elicits the same response. These results demonstrate that while Ser-113 is a substrate for p42 MAPK in vitro and can be phosphorylated in vivo as shown by Taniguchi et al. [(1994) J. Biol. Chem. 269, 18299–18302], its phosphorylation is not subject to acute regulation by p42 MAPK in Swiss 3T3 cells.

MAPK/ERK pathwayMARCKSmedicine.medical_treatmentMitogen-activated protein kinase kinaseBiochemistryenvironment and public healthSubstrate SpecificityMiceStructural BiologySerinep42MAPKinasePhosphorylationMyristoylated Alanine-Rich C Kinase SubstrateCells CulturedProtein Kinase CMitogen-Activated Protein Kinase 1Platelet-Derived Growth FactorbiologyChemistryIntracellular Signaling Peptides and Proteins3T3 CellsProtein-Tyrosine KinasesCell biologyBiochemistryMitogen-activated protein kinasePhosphorylationTetradecanoylphorbol Acetatebiological phenomena cell phenomena and immunityPlatelet-derived growth factor receptorhormones hormone substitutes and hormone antagonistsendocrine systemRecombinant Fusion ProteinsMolecular Sequence DataBiophysicsGeneticsmedicineAnimalsAmino Acid SequenceMARCKSMolecular BiologyProtein kinase CGrowth factorMembrane ProteinsProteinsCell BiologyPeptide FragmentsEnzyme ActivationMolecular Weightenzymes and coenzymes (carbohydrates)Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMutagenesis Site-DirectedMitogensFEBS letters
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A20 expression in dendritic cells protects mice from LPS-induced mortality

2014

DCs contribute to immune homeostasis under physiological conditions and regulate the immune activation during infection. The deubiquitinase A20 inhibits the activation of NF-κB-dependent immune reactions, and prevents the hyperactivation of DCs under steady-state conditions. However, the role of DC-specific A20 under pathological conditions is unknown. Here, we demonstrate that upon injection of low-dose LPS, mice with DC-specific A20 deletion (CD11c-Cre A20(fl/fl) ) died within 6 h, whereas A20(fl/fl) controls survived. LPS-induced mortality in CD11c-Cre A20(fl/fl) mice was characterized by increased serum levels of IL-2, IL-10, IL-12, IFN-γ, and TNF. Upon LPS stimulation, the activation o…

MAPK/ERK pathwayRegulation of gene expressionImmunologychemical and pharmacologic phenomenaStimulationTumor Necrosis Factor alpha-Induced Protein 3Biologymedicine.disease_causeIn vitroAutoimmunityimmune system diseasesIn vivohemic and lymphatic diseasesImmunologymedicineImmunology and AllergyTumor necrosis factor alphaEuropean Journal of Immunology
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Evaluation of the Role of Candida albicans Agglutinin-Like Sequence (Als) Proteins in Human Oral Epithelial Cell Interactions

2012

The fungus C. albicans uses adhesins to interact with human epithelial surfaces in the processes of colonization and pathogenesis. The C. albicans ALS (agglutinin-like sequence) gene family encodes eight large cell-surface glycoproteins (Als1-Als7 and Als9) that have adhesive function. This study utilized C. albicans Δals mutant strains to investigate the role of the Als family in oral epithelial cell adhesion and damage, cytokine induction and activation of a MAPK-based (MKP1/c-Fos) signaling pathway that discriminates between yeast and hyphae. Of the eight Δals mutants tested, only the Δals3 strain showed significant reductions in oral epithelial cell adhesion and damage, and cytokine pro…

MAPK/ERK pathwaySciencemedicine.medical_treatmentImmunologyBlotting WesternMycologyMicrobiologyFungal ProteinsMolecular Cell BiologymedicineGeneticsHumansPhosphorylationCandida albicansCell damageBiologyMultidisciplinarybiologyQRImmunityMouth MucosaDual Specificity Phosphatase 1Epithelial Cellsbiology.organism_classificationmedicine.diseaseCorpus albicansSignaling CascadesCell biologyBacterial adhesinCytokineImmune SystemMedicineCytokinesSignal transductionCellular TypesCandidalysinCell Adhesion MoleculesProto-Oncogene Proteins c-fosResearch ArticleDevelopmental BiologySignal Transduction
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