Search results for "Complement factor I"

showing 9 items of 9 documents

Subcellular targeting of multiligand-binding protein gC1qR.

1999

Abstract gC1q receptor, a protein originally described as the cell surface receptor for the globular heads of complement factor C1q, has been found to bind human H-kininogen with high affinity and specificity. Therefore, gC1qR has been considered candidate kininogen docking site on the surfaces of platelets, neutrophils and endothelial cells. Recent work demonstrating that gC1qR is an intracellular protein that is tightly associated with mitochondria rather than targeted to the cell surface has challenged this view. To further probe cellular trafficking routes of gC1qR, we overexpressed human gC1qR in a mammalian cell and monitored cell surface exposure of recombinant gC1qR by virtue of its…

CellComplement factor IBiologyLigandsMitochondrial ProteinsCell surface receptormedicineAnimalsHumansBinding siteReceptorPharmacologyBinding SitesMembrane GlycoproteinsBinding proteinComplement C1qBiological TransportTransfectionMolecular biologyCell biologyReceptors Complementmedicine.anatomical_structureHyaluronan ReceptorsCell cultureCOS CellsCarrier ProteinsProtein Processing Post-Translationalcirculatory and respiratory physiologySubcellular FractionsImmunopharmacology
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Binding to complement factors and activation of the alternative pathway by Acanthamoeba.

2010

Acanthamoeba can cause severe ocular and cerebral diseases in healthy and immunocompromised individuals, respectively. Activation of complement appears to play an important role in host defence against infection. The exact mechanism, however, is still unclear. The aim of the present study was to investigate the effect of normal human serum (NHS) and normal mouse serum (NMS) on Acanthamoeba trophozoites, the binding of different complement factors to Acanthamoeba and the activation of the complement system. Moreover, we aimed to work out any possible differences between different strains of Acanthamoeba. A virulent T4 strain, a non-virulent T4 strain and a virulent T6 strain were included in…

ImmunologyComplement Pathway AlternativeVirulenceAcanthamoebaComplement factor IAntigen-Antibody ComplexImmunofluorescenceMannose-Binding LectinBacterial AdhesionMicrobiologyMiceSpecies Specificityparasitic diseasesmedicineImmunology and AllergyAnimalsHumansTrophozoitesIncubationEdetic AcidMice Knockoutmedicine.diagnostic_testbiologyVirulenceComplement C1qHematologyAmebiasisComplement C3biology.organism_classificationComplement C9Complement systemAcanthamoebaMice Inbred C57BLAlternative complement pathwayIntracellularImmunobiology
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Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies

2018

The complement and coagulation cascades interact at multiple levels in thrombosis and inflammatory diseases. In venous thrombosis, complement factor 3 (C3) is crucial for platelet and tissue factor (TF) procoagulant activation dependent on protein disulfide isomerase (PDI). Furthermore, C5 selectively contributes to the exposure of leukocyte procoagulant phosphatidylserine (PS), which is a prerequisite for rapid activation of monocyte TF and fibrin formation in thrombosis. Here, we show that monoclonal cofactor-independent antiphospholipid antibodies (aPLs) rapidly activate TF on myelomonocytic cells. TF activation is blocked by PDI inhibitor and an anti-TF antibody interfering with PDI bin…

inorganic chemicals0301 basic medicineComplement factor I030204 cardiovascular system & hematologyMonocytesImmunoglobulin GThromboplastinThrombosis and HemostasisMice03 medical and health sciencesTissue factor0302 clinical medicineimmune system diseasesmedicineAnimalsPlateletneoplasmsBlood CoagulationMice KnockoutVenous ThrombosisComplement component 5biologyChemistryMonocyteComplement C5Complement C3Hematologynervous system diseasesbody regions030104 developmental biologymedicine.anatomical_structureCoagulationAntibodies Antiphospholipidbiology.proteinCancer researchAntibodyBlood Advances
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Treatment with essential amino acids in patients on chronic hemodialysis: a double blind cross-over study.

1978

Patients on chronic hemodialysis may suffer from a latent protein deficiency, and therapy with essential amino acids has been recommended. In a double blind cross-over study, 13 hemodialysis patients received orally 15.7 g of essential amino acids daily over a 3-month period. Patients were on a liberal diet, containing 1 g of protein per kilogram of body weight per day. Hemodialysis was adequate. Therapy resulted in an increase in urea, uric acid, C3 c complement factor and a fall in C4. Lysine levels increased and phenylalanine fell. Malnutrition could not account for the observed metabolic changes, which are more likely due to uremic metabolic disturbances. A liberal diet of 1 g of protei…

AdultMalemedicine.medical_specialtymedicine.medical_treatmentMedicine (miscellaneous)PhenylalanineComplement factor Ichemistry.chemical_compoundGlomerulonephritisRenal DialysisInternal medicineProtein DeficiencyMedicineHumansPrealbuminchemistry.chemical_classificationClinical Trials as TopicNutrition and DieteticsPyelonephritisbusiness.industryTransferrinComplement C3Middle Agedmedicine.diseaseCrossover studyAmino acidRetinol-Binding ProteinsMalnutritionEndocrinologychemistryBiochemistryUreaUric acidFemaleHemodialysisAmino Acids EssentialbusinessThe American journal of clinical nutrition
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Distinct contributions of complement factors to platelet activation and fibrin formation in venous thrombus development

2017

Expanding evidence indicates multiple interactions between the hemostatic system and innate immunity, and the coagulation and complement cascades. Here we show in a tissue factor (TF)-dependent model of flow restriction-induced venous thrombosis that complement factors make distinct contributions to platelet activation and fibrin deposition. Complement factor 3 (C3) deficiency causes prolonged bleeding, reduced thrombus incidence, thrombus size, fibrin and platelet deposition in the ligated inferior vena cava, and diminished platelet activation in vitro. Initial fibrin deposition at the vessel wall over 6 hours in this model was dependent on protein disulfide isomerase (PDI) and TF expressi…

0301 basic medicineComplement component 5biologyChemistryImmunologyCell BiologyHematologyComplement factor I030204 cardiovascular system & hematologymedicine.diseaseBiochemistryFibrinCell biologyComplement system03 medical and health sciences030104 developmental biology0302 clinical medicineCoagulationImmunologymedicinebiology.proteinPlateletPlatelet activationThrombusBlood
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Protein corona–mediated targeting of nanocarriers to B cells allows redirection of allergic immune responses

2018

Background Nanoparticle (NP)–based vaccines are attractive immunotherapy tools because of their capability to codeliver antigen and adjuvant to antigen-presenting cells. Their cellular distribution and serum protein interaction ("protein corona") after systemic administration and their effect on the functional properties of NPs is poorly understood. Objectives We analyzed the relevance of the protein corona on cell type–selective uptake of dextran-coated NPs and determined the outcome of vaccination with NPs that codeliver antigen and adjuvant in disease models of allergy. Methods The role of protein corona constituents for cellular binding/uptake of dextran-coated ferrous nanoparticles (DE…

0301 basic medicineendocrine systemOvalbuminCpG OligodeoxynucleotideT-Lymphocytesmedicine.medical_treatmentImmunologyMice Transgenic02 engineering and technologyComplement factor IComplement receptor03 medical and health sciencesImmune systemAntigenLectinsHypersensitivitymedicineAnimalsImmunology and AllergyFerrous CompoundsAntigensAnaphylaxisB-LymphocytesDrug CarriersMice Inbred BALB CVaccinesChemistryDextransImmunotherapyrespiratory system021001 nanoscience & nanotechnologyComplement systemMice Inbred C57BL030104 developmental biologyOligodeoxyribonucleotidesImmunologyNanoparticlesFemaleProtein Corona0210 nano-technologyAdjuvantJournal of Allergy and Clinical Immunology
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Genetic polymorphism of human complement factor I (C3b inactivator) in the Chinese Han population.

1999

The human complement factor I (IF) polymorphism has been analysed by polyacrylamide gel isoelectric focusing electrophoresis of neuraminidase-treated EDTA plasma samples followed by immunoblotting and enzymatic detection. In a population study among 121 random individuals from Chengdu, PR China, three different common phenotypes were observed. The results show that IF is polymorphic in the Chinese population. The allele frequencies were as follows: FI*A = 0.153, FI*B = 0.847. The distribution of observed phenotypes was in accordance with the Hardy-Weinberg equilibrium. In comparison to other Asian population studies, the frequency of the IF*A allele was the highest in the Chinese population…

GeneticsChinaPolymorphism GeneticGenotypeIsoelectric focusingImmunologyComplement factor IBiologyMolecular biologyEdta plasmaChinese han populationAsian PeopleComplement Factor IC3b inactivatorGeneticsHumansPolyacrylamide gel electrophoresisGenetics (clinical)AllelesExperimental and clinical immunogenetics
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Two Patients With History of STEC-HUS, Posttransplant Recurrence and Complement Gene Mutations

2013

Hemolytic uremic syndrome (HUS) is a disease of microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. About 90% of cases are secondary to infections by Escherichia coli strains producing Shiga-like toxins (STEC-HUS), while 10% are associated with mutations in genes encoding proteins of complement system (aHUS). We describe two patients with a clinical history of STEC-HUS, who developed end-stage renal disease (ESRD) soon after disease onset. They received a kidney transplant but lost the graft for HUS recurrence, a complication more commonly observed in aHUS. Before planning a second renal transplantation, the two patients underwent genetic screening for aHUS-associat…

Shiga-toxinGraft RejectionMaleDNA Primer030232 urology & nephrologyEscherichia coli InfectionGene mutationurologic and male genital diseasesGastroenterology0302 clinical medicineRecurrenceRisk Factorshemic and lymphatic diseasesImmunology and AllergyPharmacology (medical)gene mutationKidney transplantationEscherichia coli Infections0303 health sciencesKidneymedicine.diagnostic_testShiga-Toxigenic Escherichia coliAntigens CD46Microangiopathic hemolytic anemiaMiddle AgedPrognosisfemale genital diseases and pregnancy complications3. Good healthPedigreemedicine.anatomical_structureComplement Factor IComplement factor I; gene mutation; hemolytic uremic syndrome; kidney transplantation; membrane cofactor protein; Shiga-toxin; Adult; Antigens CD46; Case-Control Studies; Complement Factor I; DNA Primers; Escherichia coli Infections; Female; Genetic Testing; Graft Rejection; Hemolytic-Uremic Syndrome; Heterozygote; Humans; Kidney Failure Chronic; Kidney Transplantation; Male; Middle Aged; Mutation; Pedigree; Prognosis; Recurrence; Risk Factors; Shiga-Toxigenic Escherichia coli; Thrombocytopenia; Young Adult; Transplantation; Immunology and Allergy; Pharmacology (medical)FemaleCase-Control StudieHumanAdultmedicine.medical_specialtyHeterozygotePrognosiComplement factor IMembrane Cofactor Protein03 medical and health sciencesYoung AdultInternal medicinemedicineHumansGenetic Testing030304 developmental biologyGenetic testingDNA PrimersTransplantationbusiness.industryCD46Risk Factormedicine.diseaseKidney TransplantationThrombocytopeniaTransplantationCase-Control StudiesImmunologyHemolytic-Uremic SyndromeMutationhemolytic uremic syndromeKidney Failure ChronicbusinessAmerican Journal of Transplantation
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Binding and activation of human and mouse complement by Cryptosporidium parvum (Apicomplexa) and susceptibility of C1q- and MBL-deficient mice to inf…

2008

Cryptosporidium parvum is a protozoan parasite (Apicomplexa) that causes gastrointestinal disease in animals and humans. Whereas immunocompetent hosts can limit the infection within 1 or 2 weeks, immunocompromised individuals develop a chronic, life-threatening disease. The importance of the adaptive cellular immune response, with CD4+ T-lymphocytes being the major players, has been clearly demonstrated. Several non-adaptive immune mechanisms have been suggested to contribute to the host defence, such as interferon-gamma (IFN-gamma) from NK cells, certain chemokines, beta-defensins and pro-inflammatory cytokines, but the influence of the complement systems has been less well studied. We ana…

ChemokineImmunologyProtozoan ProteinsCryptosporidiosisComplement factor ISodium ChlorideMannose-Binding LectinMicrobiologyMiceImmune systemmedicineAnimalsHumansRNA MessengerMolecular BiologyComplement ActivationImmunodeficiencyMannan-binding lectinCryptosporidium parvumbiologyReverse Transcriptase Polymerase Chain ReactionComplement C1qOocystsTemperaturemedicine.diseasebiology.organism_classificationVirologyComplement systemMice Inbred C57BLCryptosporidium parvumGene Expression RegulationLectin pathwayComplement C3bbiology.proteinCattleDisease SusceptibilityMolecular immunology
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