Search results for "Complement Activation"

showing 10 items of 56 documents

sgp120 and the contact system in hereditary angioedema: A diagnostic tool in HAE with normal C1 inhibitor

2020

Mutations in Factor XII, plasminogen gene, angiopoietin-1 gene and kininogen 1 gene have been found in some patients with hereditary angioedema with normal C1 inhibitor (HAE-nl-C1inh), but the underlying disease mechanisms remain unclear. Additionally, there are no accepted biomarkers for this disease. Because the contact system has been implicated in hereditary angioedema with C1 inhibitor deficiency (HAE-C1inh), we studied the fragmentation patterns of serum glycoprotein 120 (sgp120), a protein that is highly susceptible to cleavage by kallikrein, in 31 HAE-C1inh and 13 HAE-nl-C1inh patient plasma samples. Compared to normal controls, the majority of plasma samples from patients with HAE-…

0301 basic medicineImmunologyProteinase Inhibitory Proteins SecretoryCleavage (embryo)C1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansKaolinComplement ActivationMolecular BiologyGenechemistry.chemical_classificationChromatographyFactor XIIbiologyChemistryAngioedemas HereditaryPlasminogenKallikreinmedicine.diseaseMolecular biologyBlood Coagulation FactorsPeptide Fragments030104 developmental biologyFactor XIIProteolysisHereditary angioedemabiology.proteinBiomarker (medicine)KallikreinsGlycoproteinComplement C1 Inhibitor ProteinPlasticsBiomarkers030215 immunologyMolecular 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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Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts

2018

Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs). Expert commentary: It is evident that aPL induce a proinflamma…

0301 basic medicineNeutrophilsImmunologyBioinformaticsExtracellular TrapsExtracellular vesiclesProinflammatory cytokinePathogenesisExtracellular VesiclesGenetic Heterogeneity03 medical and health sciences0302 clinical medicineimmune system diseasesAntiphospholipid syndromemicroRNAHumansImmunology and AllergyMedicineFetal lossBlood CoagulationComplement Activation030203 arthritis & rheumatologybusiness.industryNeutrophil extracellular trapsAntiphospholipid Syndromemedicine.diseaseMicroRNAs030104 developmental biologyAntibodies AntiphospholipidSignal transductionbusinessExpert Review of Clinical Immunology
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C3 Drives Inflammatory Skin Carcinogenesis Independently of C5

2021

Nonmelanoma skin cancer such as cutaneous squamous cell carcinoma (cSCC) is the most common form of cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinogens. There is growing evidence that the complement system is involved in cancer immune surveillance; however, its role in cSCC remains unclear. Here, we show that complement genes are expressed in tissue from patients with cSCC, and C3 activation fragments are present in cSCC biopsies, indicating complement activation. Using a range of complement-deficient mice in a two-stage mouse model of chemically-induced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutatio…

0301 basic medicineWT wild typeSkin NeoplasmsComplement receptorComplement Membrane Attack Complexmedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineCR complement receptorComplement ActivationSkinMice KnockoutcSCC cutaneous squamous cell carcinomaComplement C5Complement C3Receptors Complement030220 oncology & carcinogenesisCarcinoma Squamous CellDisease ProgressionTumor BiologyOriginal ArticleMAC membrane attack complexSignal TransductionHPV16 human papillomavirus type 16910-Dimethyl-12-benzanthraceneTPA 12-O-tetradecanoylphorbol-13-acetateMice TransgenicDermatologySettore MED/08 - Anatomia Patologica03 medical and health sciencesmedicineAnimalsHumansC3Molecular BiologyReceptor Anaphylatoxin C5aDMBA 712-dimethylbenz[a]anthracenebusiness.industry712-Dimethylbenz[a]anthraceneCancerCell BiologyNeoplasms Experimentalmedicine.diseaseComplement systemDisease Models Animal030104 developmental biologychemistryTumor progressionCancer researchCarcinogensTumor EscapeSkin cancerbusinessCarcinogenesisComplement membrane attack complexSkin carcinogenesis.EC epithelial cell
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Enzymatic modification of low-density lipoprotein in the arterial wall: a new role for plasmin and matrix metalloproteinases in atherogenesis.

2004

Objective— Functionally interactive proteases of the plasminogen/plasmin and the matrix metalloproteinase (MMP) system degrade and reorganize the extracellular matrix of the vessel wall in atherosclerosis. Here we investigated whether such proteases are able to confer atherogenic properties onto low density lipoprotein by nonoxidative modification. Methods and Results— Similar to the recently described enzymatically-modified low-density lipoprotein (E-LDL), native LDL exposed to plasmin or matrix MMP-2 or MMP-9 and cholesterylester-hydrolase (CEH) showed extensive deesterification, with ratios of free cholesterol to total cholesterol rising to 0.8 compared with 0.2 in native LDL. When the …

AdultLipoprotein modificationProteasesAdolescentPlasminArteriosclerosisBlotting WesternMatrix metalloproteinaseComplement Hemolytic Activity AssayMonocyteschemistry.chemical_compoundmedicineHumansTrypsinFibrinolysinComplement ActivationCells CulturedAgedbiologyMacrophagesAntibodies MonoclonalSodium Dodecyl SulfateLipoprotein(a)Middle AgedSterol EsteraseCell biologyLipoproteins LDLC-Reactive ProteinchemistryBiochemistryMatrix Metalloproteinase 9Low-density lipoproteinbiology.proteinMatrix Metalloproteinase 2lipids (amino acids peptides and proteins)Electrophoresis Polyacrylamide GelCardiology and Cardiovascular MedicinePlasminogen activatormedicine.drugLipoproteinArteriosclerosis, thrombosis, and vascular biology
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The impact of two whole blood inline filters on markers of coagulation, complement and cell activation

2005

Background and Objectives  There exists a current lack of information about the impact of different inline filters, used for the leucoreduction of whole blood (WB), on the levels of clotting factors and markers of coagulation, complement and cell activation in plasma. Only a few small comparisons of different types of WB inline filters have been published to date. Materials and Methods  This study compared two plasma types of 200 units each. Both study groups were derived from WB, inline-filtered and held for 2 h at 20° between donation and filtration. Then, 200 units (Group A) were filtered using a positively charged polyester filter (Baxter RZ2000) and the other 200 units (Group B) were f…

AdultMaleAdolescentFibrinogenNeutrophil ActivationThrombinmedicineHumansPlateletBlood CoagulationComplement ActivationAgedWhole bloodClotting factorChemistryHematologyGeneral MedicineMiddle AgedPlatelet ActivationMolecular biologyComplement systemImmunologyFemaleLeukocyte Reduction ProceduresCell activationBiomarkersFiltrationPlatelet factor 4medicine.drugVox Sanguinis
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C4, BF, C3 Allele Distribution and Complement Activity in Healthy Aged People and Centenarians

1999

The aim of this study was to examine the complement system and the distribution of some human leukocyte antigen (HLA) class III alleles (C4, BF) in healthy aged people (77 centenarians and 89 elderly subjects). We have also studied the alleles of C3, a complement component genetically unrelated to HLA, the immunochemical levels of C4 and C3 and serum functional hemolytic activity for classical (CH50) and alternative (AP50) complement pathway. The levels of C3 and C4 and the CH50 and AP50 were found to be within the normal range. The frequencies of C3, BF, and C4A alleles were similar in the cohorts that have been studied. For C4B null allele (C4BQ0) a trend toward an increase in the older c…

AdultMaleAgingComplement Pathway AlternativeHuman leukocyte antigenBiologyComplement Hemolytic Activity AssayHemolysisComplement factor BCohort StudiesHLA AntigensHumansComplement Pathway ClassicalAlleleComplement ActivationAllelesAgedAged 80 and overPolymorphism GeneticC4AComplement C4Complement C3DNAMiddle AgedNull alleleComplement systemImmunologyCohortFemaleGeriatrics and GerontologyGene DeletionComplement Factor BThe Journals of Gerontology Series A: Biological Sciences and Medical Sciences
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Polymorphism of the Complement C8A and -B Genes in Two Families with C8β Deficiency and Neisserial Infections

1994

Serum samples from members of two Italian families with complement C8 beta deficiency were studied by SDS-PAGE under nonreducing conditions and by IEF. The proband of family I had suffered from two episodes of purulent meningitis and two of her uncles had suffered from only one episode, while the proband of family II had suffered from three different episodes. In contrast to previous findings, where C8 beta deficiency was cosegregating with C8A (alpha-gamma) allotype A, the proband of family II had the C8A allotype B. In addition, in one of her sons a novel variant of the C8 beta chain was detected. Studies at the DNA level in family I, using a recently described PCR system, demonstrate the…

AdultMaleProbandTaqINeisseriaceae InfectionsBlotting WesternImmunologyBiologyPolymerase Chain ReactionPathology and Forensic MedicineExonchemistry.chemical_compoundHumansImmunology and AllergyAlleleComplement ActivationGeneGeneticsPolymorphism GeneticComplement C8Stop codonAllotypePedigreeRestriction sitechemistryElectrophoresis Polyacrylamide GelFemaleIsoelectric FocusingNeisseriaClinical Immunology and Immunopathology
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Synthesis of complement by macrophages and modulation of their functions through complement activation.

1983

During the last decade considerable progress has been made to characterize intimate functional links between macrophages, a major cellular component of immunoinflammatory responses, and the complement system representing the major humoral mediator of inflammation. Macrophages of various species and tissue sites have been shown to synthesize and release most of the complement components providing these cells with their own \ldpericellular\rd complement system. Circumstantial evidence for the assembly of both classical and alternative pathway convertases has been adduced. An intricate network of feedback loops involving endogenous and extrinsic factors operates to adjust complement production…

AnaphylatoxinsImmunologyComplement Pathway AlternativeGuinea PigsComplement receptorBiologyIn Vitro TechniquesMonocytesClassical complement pathwayMiceImmune systemPhagocytosisComplement C1AnimalsHumansAnaphylatoxinComplement ActivationComplement component 3MacrophagesComplement C5Complement C4General MedicineComplement C3Complement System ProteinsComplement C2Complement systemCell biologyReceptors ComplementImmunologyAlternative complement pathwayComplement C3aProstaglandinsComplement component 5aSpringer seminars in immunopathology
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Activation of the alternative pathway of complement: efficient fluid-phase amplification by blockade of the regulatory complement protein β1H through…

1981

Current concepts of activation of the alternative pathway of complement (APC) focus on the central role of an amplification mechanism triggered by C3b which is covalently bound to the surfact of activating substances. Using sulfated polyanions as model substances, an efficient fluid-phase activation of complement is demonstrated in contrast to solid-phase activation. It is shown that particulate high-molecular weight sulfated polyanions are capable of reversible binding the guinea pig and human regulatory protein beta1H. This fixation leads to an extensive activation of C3 and factor B because the regulatory function of beta1H is blocked in the fluid-phase C3b-dependent amplification system…

AnionsChemical PhenomenaComplement Pathway AlternativeGuinea PigsImmunologyBiologyComplement factor BAbsorptionGuinea pigSulfationComplement C3b Inactivator ProteinsAnimalsHumansImmunology and AllergyComplement ActivationRegulation of gene expressionChemistry PhysicalSulfatesGoatsImmune SeraComplement C3Complement systemCell biologyKineticsBiochemistryCovalent bondComplement Factor HComplement C3bAlternative complement pathwayFunction (biology)European Journal of Immunology
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