Search results for "Immune system"

showing 10 items of 2885 documents

Yeast β-glucans and microalgal extracts modulate the immune response and gut microbiome in Senegalese sole (Solea senegalensis)

2019

One bottleneck to sustainability of fish aquaculture is the control of infectious diseases. Current trends include the preventive application of immunostimulants and prebiotics such as polysaccharides. The present study investigated how yeast β-glucan (Y), microalgal polysaccharide-enriched extracts (MAe) and whole Phaeodactylum tricornutum cells (MA) modulated the gut microbiome and stimulated the immune system in Senegalese sole (Solea senegalensis) when administered by oral intubation. Blood, intestine and spleen samples were taken at 3 h, 24 h, 48 h and 7 days after treatment. The short-term response (within 48 h after treatment) consisted of up-regulation of il1b and irf7 expression in…

Chemokinebeta-GlucansRandom allocationSpleenAquatic ScienceMicrobiologyRandom Allocation03 medical and health scienceschemistry.chemical_compoundImmune systemYeast DriedmedicineMicroalgaeBeta-GlucansEnvironmental ChemistryAnimals14. Life underwaterMicrobiomeGastrointestinal microbiome030304 developmental biology2. Zero hungerDiatoms0303 health sciencesbiologyImmunity04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationAnimal FeedImmunity InnateVibrioYeastYeastGastrointestinal MicrobiomeDietmedicine.anatomical_structurePrebioticschemistry040102 fisheriesbiology.proteinFlatfishes0401 agriculture forestry and fisheriesLysozymeBacteria
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Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infe…

2008

D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6(-/-) mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor alpha, int…

Chemokinedecoy receptor inflammation Mycobacterium tuberculosis infectionmedicine.medical_treatmentInterleukin-1betaImmunologyMice TransgenicInflammationReceptors CCR10BiologyModels BiologicalArticleCCL5Proinflammatory cytokineInterferon-gammaMiceImmune systemAnti-Infective AgentsDrug Resistance BacterialmedicineAnimalsImmunology and AllergyInterferon gammaInflammationTumor Necrosis Factor-alphaArticlesMycobacterium tuberculosisPhenotypeCytokineImmune SystemImmunologybiology.proteinTumor necrosis factor alphaLymph Nodesmedicine.symptommedicine.drug
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Compartmentalized Production of CCL17 In Vivo

2003

Dendritic cells (DCs)**Abbreviations used in this paper: BM, bone marrow; CHS, contact hypersensitivity; cLN, cutaneous lymph node; CRP, C-reactive protein; DC, dendritic cell; DNFB, dinitrofluorobenzene; EGFP, enhanced green fluorescent protein; LC, Langerhans cell; LP, lamina propria; MACS, magnetic-activated cell sorting; mLN, mesenteric lymph node; ODN, oligodeoxynucleotide; PFA, paraformaldehyde; PP, Peyer's patch; TLR, Toll-like receptor; TRITC, tetramethylrhodamine-5-(and-6-)-isothiocyanate. fulfill an important regulatory function at the interface of the innate and adaptive immune system. The thymus and activation-regulated chemokine (TARC/CCL17) is produced by DCs and facilitates t…

Chemokineintegumentary systemImmunologySpleenStimulationBiologyAcquired immune systemCell biologymedicine.anatomical_structureLymphatic systemAntigenImmunologymedicinebiology.proteinImmunology and AllergyCCL17CD8Journal of Experimental Medicine
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Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

2004

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokinesMicrobes and Infection
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TLR3-induced activation of mast cells modulates CD8+ T-cell recruitment.

2005

AbstractMast cells play an important role in host defense against various pathogens, but their role in viral infection has not been clarified in detail. dsRNA, synthesized by various types of viruses and mimicked by polyinosinic-polycytidylic acid (poly(I:C)) is recognized by Toll-like receptor 3 (TLR3). In this study, we demonstrate that poly(I:C) injection in vivo potently stimulates peritoneal mast cells to up-regulate a number of different costimulatory molecules. Therefore, we examined the expression and the functional significance of TLR3 activation in mast cells. Mast cells express TLR3 on the cell surface and intracellularly. After stimulation of mast cells with poly(I:C) and Newcas…

Chemokinevirusesmedicine.medical_treatmentImmunologyNewcastle disease virusReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesBiochemistryMicemedicineCytotoxic T cellAnimalsMast CellsPhosphorylationPeritoneal CavityMice KnockoutInnate immune systemMembrane GlycoproteinsToll-Like ReceptorsCell BiologyHematologymedicine.diseaseMast cellImmunity InnateCell biologyToll-Like Receptor 3Up-RegulationMice Inbred C57BLChemotaxis Leukocytemedicine.anatomical_structureCytokinePoly I-CTLR3ImmunologyMast cell sarcomabiology.proteinCytokinesCD8Blood
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Clinical Course and Significance of the Novel FLT3-Y842C Mutation in a Patient with AML Treated with PKC412 Monotherapy.

2004

Abstract We recently identified a novel mutation (Y842C) within the tyrosine kinase domain of FLT3 in a patient treated with PKC410 monotherapy (ASH 2003, # 4681). Here, we present follow up studies including the clinical course of the patient and frequency analysis in 110 patients with AML. In addition, we characterized the novel mutation using overexpression of FLT3-Y842C in 32D cells. AML M2 was diagnosed in a 63 year old, male patient in 1993. After having experienced his second relapse upon standard therapy the patient was refractory to alemtuzumab treatment. Due to reduced performance status the patient was not eligible to standard chemotherapy and was enrolled into a phase II trial i…

ChemotherapyPerformance statusbusiness.industryPoint mutationmedicine.medical_treatmentImmunologyhemic and immune systemsCell BiologyHematologyBioinformaticsBiochemistryExonfluids and secretionshemic and lymphatic diseasesembryonic structuresCancer researchmedicineAlemtuzumabClinical significancebusinessTyrosine kinaseEx vivomedicine.drugBlood
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Definition of response to antiviral therapy in chronic hepatitis C

2000

ChemotherapyTime FactorsHepatologybusiness.industrymedicine.medical_treatmentRemission InductionFollow up studiesAntiviral therapyAlanine TransaminaseHepacivirusHepatitis C ChronicBiological effectResponse VariabilityAntiviral AgentsSensitivity and SpecificityImmune systemChronic hepatitisPredictive Value of TestsImmunologymedicineHumansRNA ViralViral diseasebusiness
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Resistance Training Safety during and after the SARS-Cov-2 Outbreak: Practical Recommendations

2020

In December of 2019, there was an outbreak of a severe acute respiratory syndrome caused by the coronavirus 2 (SARS-CoV-2 or COVID-19) in China. The virus rapidly spread into the whole world causing an unprecedented pandemic and forcing governments to impose a global quarantine, entering an extreme unknown situation. The organizational consequences of quarantine/isolation are absence of organized training and competition, lack of communication among athletes and coaches, inability to move freely, lack of adequate sunlight exposure, and inappropriate training conditions. The reduction of mobility imposed to contain the advance of the SARS-Cov-2 pandemic can negatively affect the physical con…

ChinaCoronavirus disease 2019 (COVID-19)Isolation (health care)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Pneumonia ViralRespiratory SystemBetacoronavirus; COVID-19; China; Coronavirus Infections; Disinfection; Humans; Immune System; Pneumonia Viral; Resistance Training; Respiratory System; Risk Factors; SARS-CoV-2; Safety; PandemicsReview ArticleGeneral Biochemistry Genetics and Molecular Biologylaw.inventionBetacoronavirus03 medical and health sciences0302 clinical medicineRisk FactorslawEnvironmental healthQuarantinePandemicHumansViral030212 general & internal medicinePandemicsGeneral Immunology and MicrobiologybiologySARS-CoV-2AthletesRResistance trainingCOVID-19OutbreakResistance TrainingPREVENÇÃO DE DOENÇASPneumonia030229 sport sciencesGeneral Medicinebiology.organism_classificationDisinfectionImmune SystemMedicineBetacoronavirus COVID-19 China Coronavirus Infections Disinfection Humans Immune System Pneumonia Viral Resistance Training Respiratory System Risk Factors SARS-CoV-2 Safety PandemicsBusinessSafetyCoronavirus InfectionsBioMed Research International
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Cholera-Like Enterotoxins and Regulatory T cells

2010

Cholera toxin (CT) and the heat-labile enterotoxin of E. coli (LT), as well as their non toxic mutants, are potent mucosal adjuvants of immunization eliciting mucosal and systemic responses against unrelated co-administered antigens in experimental models and in humans (non toxic mutants). These enterotoxins are composed of two subunits, the A subunit, responsible for an ADP-ribosyl transferase activity and the B subunit, responsible for cell binding. Paradoxically, whereas the whole toxins have adjuvant properties, the B subunits of CT (CTB) and of LT (LTB) have been shown to induce antigen specific tolerance when administered mucosally with antigens in experimental models as well as, rece…

Cholera ToxinHealth Toxicology and Mutagenesismedicine.medical_treatmentBacterial Toxinslcsh:MedicineEnterotoxinReviewBiologyToxicologymedicine.disease_causeT-Lymphocytes Regulatoryregulatory T cellsMicrobiologyImmune toleranceAutoimmune DiseasesEnterotoxinsImmune systemAntigenAdjuvants ImmunologicmedicineImmune ToleranceAnimalsHumansAntigen-presenting cellEscherichia coli Proteinslcsh:RCholera toxinCTBIn vitroLTBImmunologyAdjuvantheat-labile enterotoxin of E. colicholera-like enterotoxinsToxins
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Triggers of Exacerbation in Chronic Urticaria and Recurrent Angioedema—Prevalence and Relevance

2021

Patients with urticaria and angioedema often have triggers that cause an outbreak or a swelling episode or worsen their chronic condition. Exploring these factors with each patient may result in better understanding and control of their disease. Patients should be advised to avoid known triggers, if feasible, or prepare to prevent or control an exacerbation with appropriate pretreatment if avoidance is not possible. In this review, we describe and discuss a variety of factors for which there is evidence that they cause or exacerbate chronic spontaneous urticaria and angioedema. These potentially exacerbating factors include drugs, food additives, and naturally occurring pseudoallergens, men…

Chronic conditionmedicine.medical_specialtyUrticariaExacerbationDiseaseImmunoglobulin EC1-inhibitor03 medical and health sciences0302 clinical medicineimmune system diseasesPrevalencemedicineHumansImmunology and AllergyChronic Urticaria030212 general & internal medicineAngioedemaskin and connective tissue diseasesIntensive care medicineChronic urticariabiologyAngioedemabusiness.industrymedicine.disease030228 respiratory systemChronic DiseaseHereditary angioedemabiology.proteinmedicine.symptombusinessThe Journal of Allergy and Clinical Immunology: In Practice
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