Search results for "NOD1"

showing 4 items of 4 documents

NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

2019

Innate immunity comprises several inflammation-related modulatory pathways which receive signals from an array of membrane-bound and cytoplasmic pattern recognition receptors (PRRs). The NLRs (NACHT (NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from Podospora anserina) and TP1 (telomerase-associated protein) and Leucine-Rich Repeat (LRR) domain containing proteins) relate to a large family of cytosolic innate receptors, involved in detection of intracellular pathogens and endogenous byproducts of tissue injury. These receptors may recognize pathogen-associated molecular patterns (PAMPs) and/or danger-associated…

0301 basic medicineNOD1InflammasomesBiophysicsNLR ProteinsReview ArticleRECEPTORESBiochemistry46NOD2NLR Proteins45NLRInflammasome03 medical and health sciences0302 clinical medicineNeoplasmsMHC class INOD1medicineAnimalsHumansNF-kBReceptorMolecular BiologyReview ArticlesCancerInflammationInnate immune systembiologyPathogen-Associated Molecular Pattern MoleculesPattern recognition receptorNF-kappa BInflammasomeCell Biology3910Immunity InnateCell biology030104 developmental biology030220 oncology & carcinogenesisReceptors Pattern Recognitionbiology.proteinNAIPmedicine.drug
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Bronchial inflammation and bacterial load in stable COPD is associated with TLR4 overexpression.

2017

Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial muc…

0301 basic medicineTIRAPMaleRespiratory SystemVital CapacityHAEMOPHILUS-INFLUENZAELUNG MICROBIOMEPathogenesisPulmonary Disease Chronic Obstructive0302 clinical medicineNOD2ImmunopathologyForced Expiratory VolumeNod1 Signaling Adaptor ProteinNOD1PhosphorylationCOPDSmoking11 Medical And Health SciencesMiddle AgedCPG-DNAbronchial inflammationAnti-Bacterial AgentsStreptococcus pneumoniaePseudomonas aeruginosaMOUSE LUNGFemaleLife Sciences & BiomedicineMoraxella catarrhalisSignal TransductionEXPRESSIONPulmonary and Respiratory MedicineCD14BronchiRespiratory MucosaReal-Time Polymerase Chain ReactionOBSTRUCTIVE PULMONARY-DISEASETLRs NLR bronchial inflammationNLRDENDRITIC CELL SUBSETS03 medical and health sciencesProtein DomainsmedicineHumansTLRsAgedTOLL-LIKE RECEPTORSCOPD TLR4InflammationScience & TechnologyBacteriabusiness.industrymedicine.diseaseHaemophilus influenzaeBacterial Loadrespiratory tract diseasesToll-Like Receptor 4TLR2030104 developmental biology030228 respiratory systemImmunologyINNATE IMMUNITYT-CELLSbusinessThe European respiratory journal
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Anaplasma phagocytophilum Induces TLR- and MyD88-Dependent Signaling in In Vitro Generated Murine Neutrophils

2021

Anaplasma phagocytophilum is a tick-transmitted obligate intracellular Gram-negative bacterium that replicates in neutrophils. It elicits febrile disease in humans and in animals. In a mouse model, elimination of A. phagocytophilum required CD4+ T cells, but was independent of IFN-γ and other classical antibacterial effector mechanisms. Further, mice deficient for immune recognition and signaling via Toll-like receptor (TLR) 2, TLR4 or MyD88 were unimpaired in pathogen control. In contrast, animals lacking adaptor molecules of Nod-like receptors (NLR) such as RIP2 or ASC showed delayed clearance of A. phagocytophilum. In the present study, we investigated the contribution of further pattern…

0301 basic medicineMicrobiology (medical)ChemokineCLRanimal diseasesImmunologylcsh:QR1-502Microbiologylcsh:MicrobiologyNLR03 medical and health sciencesCellular and Infection Microbiology0302 clinical medicineImmune systemTLRparasitic diseasesNOD1cytokineddc:610ReceptorOriginal ResearchbiologychemokinefungiPattern recognition receptorSignal transducing adaptor proteinMyD88bacterial infections and mycosesbiology.organism_classificationAnaplasma phagocytophilumCell biologyiNOS030104 developmental biologyInfectious DiseasesTLR4biology.proteinbacteriaAnaplasma phagocytophilum030215 immunologyFrontiers in Cellular and Infection Microbiology
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Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence…

2011

Abstract Background Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>…

AdultGastritis AtrophicMaleFas Ligand ProteinGenotypeAtrophic gastritisPeptidyl-Dipeptidase AWhite PeopleFas ligandHelicobacter InfectionsRisk FactorsStomach NeoplasmsNod1 Signaling Adaptor ProteinNOD1GenotypemedicineGeneticsHumansGenetics(clinical)fas ReceptorAllelesGenetics (clinical)AgedAged 80 and overPolymorphism GeneticHelicobacter pyloribiologyCancerAngiotensin-converting enzymeMiddle AgedHelicobacter pylorimedicine.diseasebiology.organism_classificationToll-Like Receptor 4ApoptosisImmunologybiology.proteinFemalePrecancerous ConditionsResearch ArticleBMC Medical Genetics
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