Search results for "toll-like receptors"

showing 10 items of 70 documents

Toll-like receptors and autoimmunity

2008

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. This review will focus on TLRs 7, 8 and 9 which were originally iden…

Regulation of gene expressionToll-Like ReceptorsImmunologyReceptors Antigen B-CellRNAAutoimmunityContext (language use)Dendritic CellsBiologymedicine.disease_causeAutoimmunitychemistry.chemical_compoundImmune systemGene Expression RegulationAntigenchemistryImmunologymedicineHumansImmunology and AllergyReceptorDNAAutoimmunity Reviews
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Pathogenetic Mechanisms of Hypertension-Brain-Induced Complications: Focus on Molecular Mediators.

2021

There is growing evidence that hypertension is the most important vascular risk factor for the development and progression of cardiovascular and cerebrovascular diseases. The brain is an early target of hypertension-induced organ damage and may manifest as stroke, subclinical cerebrovascular abnormalities and cognitive decline. The pathophysiological mechanisms of these harmful effects remain to be completely clarified. Hypertension is well known to alter the structure and function of cerebral blood vessels not only through its haemodynamics effects but also for its relationships with endothelial dysfunction, oxidative stress and inflammation. In the last several years, new possible mechani…

Settore MED/09 - Medicina InternaOrganic ChemistryToll-Like ReceptorsHemodynamicsBrainGeneral MedicineCatalysisCerebral complications Endothelial dysfunction Hypertension Innate immune system Neuroinflammation Oxidative stress Toll-like receptorsImmunity InnateComputer Science ApplicationsInorganic ChemistryOxidative StressHypertensionDisease ProgressionAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologySpectroscopyInternational journal of molecular sciences
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Synergistic activation of dendritic cells by combined Toll-like receptor ligation induces superior CTL responses in vivo.

2006

Toll-like receptors (TLRs) are able to interact with pathogen-derived products and their signals induce the coordinated activation of innate and adaptive immune mechanisms. Dendritic cells (DCs) play a central role in these events. As the different TLRs are able to trigger MyD88/TRIF-dependent and -independent signaling pathways, we wondered if the simultaneous activation of these signaling cascades would synergize with respect to DC activation and induce superior cytotoxic T-lymphocyte (CTL) activity in vivo. We observed that indeed the combined activation of MyD88-dependent and -independent signaling induced by TLR7 and TLR3 ligands provoked a more rapid and more sustained bone marrow–der…

T-LymphocytesImmunologyBone Marrow CellsBiologyLigandsBiochemistryT-Lymphocytes RegulatoryMiceCytotoxic T cellAnimalsAntigen-presenting cellAdaptor Proteins Signal TransducingCD86Toll-like receptorCD40Membrane GlycoproteinsToll-Like ReceptorsImmunityhemic and immune systemsCell BiologyHematologyDendritic cellDendritic CellsAcquired immune systemCell biologyToll-Like Receptor 3Mice Inbred C57BLCTL*Toll-Like Receptor 7ImmunologyMyeloid Differentiation Factor 88biology.proteinSignal TransductionT-Lymphocytes CytotoxicBlood
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Talin1 sets the stage for dendritic cell activation

2020

In dendritic cells, talin1 links integrin binding to efficient TLR downstream signaling through interaction with MyD88 and PIP5K.

TalinCellular differentiationImmunologyIntegrinInsightsMiceConditional gene knockoutImmune ToleranceImmunology and AllergyAnimalsSkinMice KnockoutMembrane GlycoproteinsbiologyChemistryChemotaxisToll-Like ReceptorsNF-kappa BReceptors Interleukin-1Dendritic cellCell biologyPhosphotransferases (Alcohol Group Acceptor)Langerhans CellsMyeloid Differentiation Factor 88biology.proteinCytokinesSignal transductionSignal TransductionThe Journal of Experimental Medicine
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Damping excessive inflammation and tissue damage in Mycobacterium tuberculosis infection by Toll IL-1 receptor 8/single Ig IL-1-related receptor, a n…

2007

Abstract Toll IL-1R 8/single Ig IL-1-related receptor (TIR8/SIGIRR) is a member of the IL-1R family, expressed by epithelial tissues and immature dendritic cells, and is regarded as a negative regulator of TLR/IL-1R signaling. Tir8-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis, despite controlling efficiently the number of viable bacilli in different organs. Tir8−/−-infected mice showed an increased number of neutrophils and macrophages in the lungs; however, mycobacteria-specific CD4 and CD8 T cells were similar in Tir8−/− and Tir8+/+ mice. Exaggerated mortality of Tir8−/− mice was due to massive liver necrosis and was accompanie…

TuberculosisNeutrophilsImmunologyInterleukin-1betaInflammationBiologyPeripheral blood mononuclear cellAntibodiesMycobacterium tuberculosisMiceNecrosisCell MovementMacrophages AlveolarmedicineImmunology and AllergyCytotoxic T cellAnimalsReceptorLungTuberculosis PulmonaryInflammationLungTumor Necrosis Factor-alphaToll-Like ReceptorsReceptors Interleukin-1Dendritic CellsMycobacterium tuberculosismedicine.diseasebiology.organism_classificationIn vitroMice Mutant Strainsmedicine.anatomical_structureLiverImmunologyCytokinesmedicine.symptomToll IL-1 Receptor 8/Single Ig IL-1-Related Receptor Inlfammation Mycobacterium tuberculosisInterleukin-1Signal Transduction
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Toll signal transduction pathway in bivalves: Complete cds of intermediate elements and related gene transcription levels in hemocytes of immune stim…

2014

Based on protein domain structure and organization deduced from mRNA contigs, 15 transcripts of the Toll signaling pathway have been identified in the bivalve, Mytilus galloprovincialis. Identical searches performed on publicly available Mytilus edulis ESTs revealed 11 transcripts, whereas searches performed in genomic and new transcriptome sequences of the Pacific oyster, Crassostrea gigas, identified 21 Toll-related transcripts. The remarkable molecular diversity of TRAF and IKK coding sequences of C. gigas, suggests that the sequence data inferred from Mytilus cDNAs may not be exhaustive. Most of the Toll pathway genes were constitutively and ubiquitously expressed in M. galloprovinciali…

animal structuresMolluskToll signaling pathwayInnate immunity; Mollusks; Mytilus; Signal transduction; Toll pathway; NF-κBImmunologyProtein domainSettore BIO/05 - ZoologiaMytiluSignal transductionNF-κBTranscriptomeTranscription (biology)Animals[SDU.STU.HY]Sciences of the Universe [physics]/Earth Sciences/HydrologyGenePhylogenyComputingMilieux_MISCELLANEOUSMytilusInnate immunityMessenger RNAInnate immune systemMollusksToll-like receptors; signal transduction; Mytilus-galloprovincialis Lmk (bivalvia)biologyEcologyfungiMytilus-galloprovincialis Lmk (bivalvia)biology.organism_classificationMytilusToll-like receptorsCell biologyInnate immunity; Mollusks; Mytilus; NF-κB; Signal transduction; Toll pathwayToll pathwayNF-jBDevelopmental Biology
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Cigarette smoke increases TLR4 and modifies LPS 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 Tolllike 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-jB (NF-jB) 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 both NF-jB a…

cigarette smokeSettore MED/10 - Malattie Dell'Apparato Respiratorioairway epithelial cellToll-like receptors
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Immunology of human rickettsial diseases.

2008

Among human rickettsial diseases caused by micro-organisms of the genus Rickettsia (Order Rickettsiales; Family Rickettsiaceae), transmitted to human hosts through arthropod vectors, Mediterranean Spotted Fever, or Boutonneuse Fever, and Rocky Mountain Spotted Fever are considered to be important infectious diseases due to continued prevalence in the developed world, and potentially fatal outcome in severe cases. Proliferation of rickettsiae, at the site of the tick bite, results in focal epidermal and dermal necrosis (tache noire). Rickettsiae then spread via lymphatic vessels to the regional lymph nodes, and, via the bloodstream, to skin, brain, lungs, heart, liver, spleen and kidneys. Th…

immunologySettore MED/09 - Medicina InternaToll-Like Receptorsimmunology; rickettsiaEndothelial CellsHumansRickettsia InfectionsCD8-Positive T-LymphocytesAcute-Phase ReactionrickettsiaImmunity Innate
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Are Toll-like receptors and decoy receptors involved in the immunopathogenesis of systemic lupus erythematosus and lupus-like syndromes?

2011

In this paper we focus our attention on the role of two families of receptors, Toll-like receptors (TLR) and decoy receptors (DcR) involved in the generation of systemic lupus erythematosus (SLE) and lupus-like syndromes in human and mouse models. To date, these molecules were described in several autoimmune disorders such as rheumatoid arthritis, antiphospholipids syndrome, bowel inflammation, and SLE. Here, we summarize the findings of recent investigations on TLR and DcR and their role in the immunopathogenesis of the SLE.

lcsh:Immunologic diseases. AllergyChemokineImmunologyInflammationAutoimmunityReview ArticleCell Communicationmedicine.disease_causeAutoantigensAutoimmunityMiceimmune system diseasesToll-like receptormedicineImmunology and AllergyAnimalsHumansLupus Erythematosus SystemicDecoy receptorsReceptorskin and connective tissue diseasesSettore MED/04 - Patologia GeneraleToll-like receptors decoy receptors systemicic erythematous lupusSystemic lupus erythematosusbiologybusiness.industryToll-Like ReceptorsGeneral Medicinemedicine.diseaseImmunity Innatedecoy receptorDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsRheumatoid arthritisImmunologybiology.proteinsystemicic erythematous lupusmedicine.symptomChemokinesbusinesslcsh:RC581-607Tumor Necrosis Factor Decoy ReceptorsSignal Transduction
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Mucin 1 downregulation associates with corticosteroid resistance in chronic rhinosinusitis with nasal polyps

2013

Background A number of patients with chronic rhinosinusitis with nasal polyps (CRSwNP) are resistant to oral corticosteroids. Mucin 1 (MUC1) shows anti-inflammatory properties, and its cytoplasmic tail (CT) interacts with transcription factors, facilitating their nuclear translocation. Because glucocorticoid receptor (GR) nuclear translocation is key to the anti-inflammatory effect of corticosteroids, we hypothesized that MUC1 is involved in the effectiveness of corticosteroids. Objective To analyze the role of MUC1 in corticosteroid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved. Methods Seventy-three patients with CRSwNP took oral…

medicine.drug_classImmunologyAnti-Inflammatory AgentsDrug ResistanceDown-Regulationdigestive systemNasal PolypsReceptors GlucocorticoidGlucocorticoid receptorDownregulation and upregulationAdrenal Cortex HormonesmedicineHumansImmunology and AllergyNasal polypsSinusitisskin and connective tissue diseasesneoplasmsDexamethasoneMUC1Rhinitisbusiness.industryMucin-1Toll-Like ReceptorsMucinmedicine.diseasebiological factorsdigestive system diseasesNasal MucosaGene Expression RegulationChronic DiseaseImmunologyImmunohistochemistryCorticosteroidbusinessSignal Transductionmedicine.drugJournal of Allergy and Clinical Immunology
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