Search results for "Complement System"

showing 10 items of 157 documents

Physicochemical characterization of the fifth (C5), sixth (C6), seventh (C7), eighth (C8) and ninth (C9) component of guinea pig complement.

1971

A physicochemical characterization of the purified guinea pig complement components C5 to C9 is given. For this purpose the sedimentation rate, the diffusion coefficient, the molecular weight and the isoelectric point were determined and compared with the values already known for the guinea pig and human complement system. For the determination of the physicochemical parameters gel filtration on Sephadex G-200, ultracentrifugation applying a sucrose density gradient and thin-layer isoelectric focusing were used. By comparing the values of the human and guinea pig complement a remarkable similarity is shown.

ErythrocytesDensity gradientChemical PhenomenaImmunologySize-exclusion chromatographyGuinea PigsBiologyGuinea pigHemoglobinsCentrifugation Density GradientImmunology and AllergyAnimalsHumansChromatographyIsoelectric focusingChemistry PhysicalVenomsElectric ConductivitySnakesComplement System ProteinsCatalaseComplement systemMolecular WeightIsoelectric pointSephadexImmunoglobulin GImmunologyChromatography GelUltracentrifugeIsoelectric FocusingEuropean journal of immunology
researchProduct

Role of C-reactive protein in atherogenesis: can the apolipoprotein E knockout mouse provide the answer?

2005

Objective—Human C-reactive protein (CRP) was reported to accelerate atherosclerotic lesion development in male but not in female apolipoprotein E (apoE) knockout mice. Here, mice expressing rabbit CRP (rbCRP) were crossbred onto apoE knockout animals, and the effect on atherogenesis was studied.Methods and Results—Hemolytic complement activity could not be detected in apoE knockout mice. Furthermore, in contrast to human complement, neither rabbit nor human CRP complexed to modified low-density lipoprotein–activated murine complement. At 52 weeks, rbCRP levels were similar in male and female transgenic animals. Serum cholesterol levels were equivalent in female animals irrespective of rbCRP…

Apolipoprotein EMalemedicine.medical_specialtyPathologyRatónTransgeneHypercholesterolemiaMice TransgenicLesionMiceApolipoproteins ESpecies SpecificityInternal medicinemedicineAnimalsHumansTransgenesAortaMice KnockoutbiologyVascular diseaseC-reactive proteinCholesterol LDLComplement System Proteinsmedicine.diseaseAtherosclerosisComplement systemMice Inbred C57BLDisease Models AnimalEndocrinologyC-Reactive ProteinKnockout mousebiology.proteinFemaleDietary ProteinsRabbitsmedicine.symptomCardiology and Cardiovascular MedicineArteriosclerosis, thrombosis, and vascular biology
researchProduct

T cell factor (interleukin 2) allows in vivo induction of T helper cells against heterologous erythrocytes in athymic (nu/nu) mice.

1980

Mice carrying the nude mutation (nu/nu) lack a functioning thymus and do not contain detectable levels of immunocompetent T cells. We now report that nu/nu mice do have lymphocytes which can be activated in vivo by heterologous erythrocytes and a Lyt-1 T cell-derived factor (interleukin 2) to generate T helper cells. Thus, a lymphokine is described which is able to restore in vivo T helper cell immunocompetence of nu/nu mice. The data may suggest that nu/nu mice contain a low number of T lymphocytes influenced by the cystic remnant of the nu/nu thymus anlage. Alternatively, the data imply that interleukin 2 circumvents the requirement of a thymus during ontogeny of T lymphocytes.

Interleukin 2ErythrocytesT cellT-LymphocytesImmunologyHeterologousMice NudeBiologymedicine.disease_causeMiceIn vivomedicineImmunology and AllergyAnimalsAntilymphocyte SerumMutationMice Inbred C3HSheepLymphokineT helper cellComplement System ProteinsMolecular biologyMice Inbred C57BLmedicine.anatomical_structureImmunologyImmunocompetencemedicine.drugEuropean journal of immunology
researchProduct

Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
researchProduct

Thrombotic risk in paroxysmal nocturnal hemoglobinuria-like (PNH-like) phenotype

2020

The complement system is an essential component of the innate immune defence that, if overly activated, may damage organs and tissues. For this reason, there is a fine complement regulatory system. The complement modulation system includes two proteins with important regulatory activity, CD55 or decay accelerating factor (DAF) and CD59 or membrane inhibitor of reactive lysis (MIRL). The paroxysmal nocturnal hemoglobinuria (PNH) is a clonal and non-neoplastic disease characterized by intravascular haemolysis, occurrence of thrombosis and bone marrow failure. In clinical practice, in opposition to PNH, a variety of pathological conditions have been observed with an acquired and non-genetic de…

PhysiologyHemoglobinuria ParoxysmalDiseaseCD59030204 cardiovascular system & hematologyHemolysis030218 nuclear medicine & medical imagingSettore MED/15 - Malattie Del Sangue03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)medicineHumansParoxysmal nocturnal hemoglobinuriaDecay-accelerating factorcomplement systemInnate immune systembusiness.industryThrombosisHematologythromboembolic riskmedicine.diseasePhenotypeComplement systemPhenotypemedicine.anatomical_structureImmunologyParoxysmal nocturnal hemoglobinuriaBone marrowCD55Cardiology and Cardiovascular MedicinebusinessCD59
researchProduct

The apolipoprotein(a) moiety of lipoprotein(a) interacts with the complement activation fragment iC3b but does not functionally affect C3 activation …

1992

A previous study has shown that complement component C3 binds to recombinant apolipoprotein(a) (r-apo(a)). In the present report we have investigated the interactions between lipoprotein(a) (Lp(a)), r-apo(a) and C3 in relation to complement activation and degradation. Neither Lp(a) nor r-apo(a) affected complement activation as indicated by sheep and rabbit red blood cell hemolytic assays, and by assessment of the amount of C3a generated in zymosan-activated human serum in the presence or absence of Lp(a). Crossed immunoelectrophoretic analyses indicated that Lp(a) retarded the migration of iC3b in complement-activated serum but had no effects on C3, C3b, C3c or C3dg. Recombinant apo(a) exh…

Apolipoprotein BLipoproteinsApoprotein(a)chemistry.chemical_compoundHumansComplement ActivationbiologyComplement C3Lipoprotein(a)N-Acetylneuraminic AcidComplement systemSialic acidApolipoproteinsBiochemistrychemistryLow-density lipoproteinComplement C3bSialic Acidsbiology.proteiniC3bElectrophoresis Polyacrylamide Gellipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineImmunoelectrophoresis Two-DimensionalN-Acetylneuraminic acidLipoprotein(a)LipoproteinAtherosclerosis
researchProduct

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
researchProduct

C1q secreted in the tumour microenvironment promotes tumour growth in the absence of complement activation

2012

We have recently shown that locally secreted C1q is involved in trophoblast invasion of decidua during pregnancy (Agostinis et al., J. Immunol. 2010;185;4420–4429). Since this physiologic process resembles to some extent tumor progression, we sought to investigate if C1q plays a similar role in tumor development and progression. Immunohistochemical analysis of several solid tumours including colon, prostate, lung and breast cancer and melanoma revealed the presence of C1q that was localized on the vascular endothelium and also distributed in the stroma in the absence of C4. To investigate the in vivo role of C1q in tumour development, 6/8 week old female WT and C1q−/− C57BL/6 mice received …

ChemistrytumourImmunologyImmunology and AllergycomplementHematologycomplement; tumourComplement systemComplement (complexity)Cell biology
researchProduct

The modulation of immune complex aggregation by classical pathway-mediated reactions.

1985

Abstract Classical pathway (CP)-triggered reactions of complement-modulated immune complex(IC) aggregation (tetanus toxoid/human anti-tetanus toxoid-IgG; ICs of equivalence) were investigated turbidimetrically during the early stages of reaction. Monospecific Fab'- or Fab-fragments (rabbit) directed against certain complement components were used to block the complement function in normal human serum (NHS). Additionally, parts of the reactions were studied using purified complement components. C1q in serum generated by the addition of EDTA as well as purified C1q were found to increase the IC aggregation. In contrast to C1q, macromolecular C1 is able to inhibit IC aggregation, whereas addit…

EffectorChemistryComplement Activating EnzymesComplement C1qImmunologyToxoidHematologyAntigen-Antibody ComplexComplement System ProteinsComplement C1 Inactivator ProteinsImmune complexComplement componentsComplement (complexity)Classical complement pathwayBiochemistrySolubilityComplement C1ImmunologyImmunology and AllergyHumansComplement Pathway ClassicalComplement ActivationFunction (biology)MacromoleculeImmunobiology
researchProduct

Structural characterization of CspZ, a complement regulator factor H and FHL-1 binding protein fromBorrelia burgdorferi

2014

Borrelia burgdorferi is the causative agent of Lyme disease and is found in two different types of hosts in nature - Ixodes ticks and various mammalian organisms. To initiate disease and survive in mammalian host organisms, B. burgdorferi must be able to transfer to a new host, proliferate, attach to different tissue and resist the immune response. To resist the host's immune response, B. burgdorferi produces at least five different outer surface proteins that can bind complement regulator factor H (CFH) and/or factor H-like protein 1 (CFHL-1). The crystal structures of two uniquely folded complement binding proteins, which belong to two distinct gene families and are not found in other bac…

Lyme DiseaseIxodesbiologyBinding proteinMutagenesis (molecular biology technique)Cell Biologycomputer.file_formatVinculinProtein Data Bankbiology.organism_classificationBiochemistryDNA-binding proteinComplement systemMicrobiologyCell biologyBacterial ProteinsBorrelia burgdorferibiology.proteinAnimalsGene familyBorrelia burgdorferiMolecular BiologycomputerFEBS Journal
researchProduct