Search results for "Complement C1q"

showing 10 items of 51 documents

Autoreactivity to mouse C1q in a murine model of SLE.

1995

A large proportion of systemic lupus erythematosus (SLE) patients develop glomerulonephritis, coincident with the appearance of autoantibodies to C1q, the Fc-recognizing collagen-like subcomponent of the first component of complement, C1. The MRL/lpr/lpr mouse is an established model for SLE, developing both antinuclear and anti-type II collagen autoantibodies, and rheumatoid factors(s), exhibiting reduced complement levels and later on developing glomerulonephritis and often arthritis. We report here an age-dependent decrease in serum C1q levels coincident with the development of IgG2b autoantibodies reactive with mouse C1q in MRL/lpr/lpr mice. Unlike IgG2b, although high levels of IgM, Ig…

Systemic diseaseImmunologyArthritischemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent Assayurologic and male genital diseasesmedicine.disease_causeAutoimmunityMiceRheumatologyimmune system diseasesImmunology and AllergyMedicineAnimalsLupus Erythematosus Systemicskin and connective tissue diseasesAutoantibodiesLupus erythematosusbusiness.industryComplement C1qAutoantibodyGlomerulonephritismedicine.diseaseConnective tissue diseaseLupus NephritisDisease Models AnimalImmunologybusinessAnti-SSA/Ro autoantibodiesRheumatology international
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A longitudinal study of C1q and anti-C1q autoantibodies in homologous and heterologous pregnancies for predicting pre-eclampsia

2022

C1q, the recognition molecule of the classical pathway of the complement system, plays a central role in pregnancy. Lack of C1q is characterized by poor trophoblast invasion and pregnancy failure. C1q can be the target of an antibody response: anti‐C1q autoantibodies (anti-C1q) are present in several infectious and autoimmune diseases. The presence of these autoantibodies has been detected also in 2-8% of the general population. Recent evidence indicates that women who undergo assisted reproductive technology (ART) have an increased risk of developing pre-eclampsia (PE), particularly oocyte donation (OD) pregnancies. The aim of this study was to characterize the levels of C1q and anti-C1q i…

anti-C1q autoantibodiepre-eclampsiaART pregnancy; C1q; anti-C1q autoantibodies; oocyte donation; pre-eclampsia; Female; Humans; Pregnancy; Autoantibodies; Complement C1q; Longitudinal Studies; Placenta; Pre-Eclampsiapre-eclampsia.Complement C1qPlacentaImmunologyanti-C1q autoantibodiesLongitudinal StudieART pregnancySettore MED/08 - Anatomia PatologicaAutoantibodiePre-EclampsiaPregnancyoocyte donationSettore MED/05 - Patologia ClinicaImmunology and AllergyHumansFemaleLongitudinal StudiesC1qAutoantibodiesHuman
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Studies on the interaction of C1q,a subcomponent of the first component of complement, with porins fromSalmonella minnesotaincorporated into artifici…

1990

AbstractPurified outer membrane proteins (OMP) of Salmonella minnesota, Re-form, were incorporated into liposomes. These induced in macrophages a chemiluminescence signal identical to that of the intact Re-form. This signal was abolished by preincubation of porin-containing liposomes with purified C1q. Incorporation of isolated OMP into black lipid membranes (BLM) resulted in channel-formation which could not be inhibited by isolated C1q. Additionally, incubation of OMP-containing liposomes with BLM resulted in pore-formation within the BLM. This was amplified when lipid A was present within the liposomes. Preincubation of OMP-containing liposomes with purified C1q abolished pore-formation …

congenital hereditary and neonatal diseases and abnormalitiesLuminescenceMacrophageLipid BilayersBiophysicsSynthetic membranePorinschemical and pharmacologic phenomenaBiochemistryIon ChannelsMembrane PotentialsLipid AMiceSalmonellaStructural BiologyGeneticsAnimalsHumansBlack lipid membraneLipid bilayerMolecular BiologyC1qCells CulturedMice Inbred BALB CLiposomeurogenital systemChemistryComplement C1qMacrophagesElectric Conductivitynutritional and metabolic diseasesMembranes ArtificialCell BiologyLiposomeKineticsCholesterolMembraneMembrane proteinBiochemistryOuter membrane proteinPorinPhosphatidylcholinesbacteriaBacterial outer membraneBacterial Outer Membrane ProteinsFEBS Letters
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Is the Complement Protein C1q a Pro- or Anti-tumorigenic Factor? Bioinformatics Analysis Involving Human Carcinomas

2019

C1q is the first subcomponent of the classical pathway of the complement system and belongs to the C1q/Tumor Necrosis Factor superfamily. C1q can perform a diverse range of immune and non-immune functions in a complement-dependent as well as -independent manner. Being a pattern recognition molecule of the innate immunity, C1q can recognize a number of self, non-self and altered-self ligands and bring about effector mechanisms designed to clear pathogens via opsonisation and inflammatory response. C1q is locally synthesized by macrophages and dendritic cells, and thus, can get involved in a range of biological processes, such as angiogenesis and tissue remodeling, immune modulation, and immu…

lcsh:Immunologic diseases. Allergy0301 basic medicinetumorLung NeoplasmsMicroenvironmentPrognosiImmunologyComplementBreast Neoplasmschemical and pharmacologic phenomenaKaplan-Meier EstimateBiology03 medical and health sciencesClassical complement pathway0302 clinical medicineImmune systemimmune system diseasesmedicineHumansImmunology and Allergycomplementclassical pathwayskin and connective tissue diseasesC1qOriginal ResearchTumorInnate immune systemEffectorComplement C1qComputational BiologyCancerPrognosismedicine.diseasemicroenvironmentKidney NeoplasmsComplement systemClear cell renal cell carcinomaC1q; Classical pathway; Complement; Microenvironment; Prognosis; Tumor030104 developmental biologyClassical pathwayCancer researchAdenocarcinomaprognosislcsh:RC581-607030215 immunologyFrontiers in Immunology
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Molecular cloning and characterization of the complementary DNA coding for the B-chain of murine Clq

1989

AbstractcDNA clones coding for the B-chain of murine Clq were isolated from a mouse macrophage library. The characterized clones include the total coding region plus a leader sequence. High homology was found with human Clq B-chain in the coding region (81%). Northern blot analysis of total RNA from different tissues of Balb/c mice showed one band of approximately 1.2 kb. The highest signal was found in RNA preparations of thioglycolate-activated peritoneal macrophages. The probe also hybridized with mRNA from spleen, thymus and heart. Extremely weak signals were found in liver, kidney, lung and intestine tissues.

mRNAMolecular Sequence DataBiophysicsProtein Sorting SignalsMolecular cloningBiologyBiochemistryMiceStructural BiologySequence Homology Nucleic AcidComplementary DNAGeneticsAnimalsHumansCoding regionGenomic libraryRNA MessengerNorthern blotCloning MolecularPromoter Regions GeneticMolecular BiologyGeneMice Inbred BALB CMessenger RNAComplement C1qNucleic Acid HybridizationRNADNARNA ProbesCell BiologyBlotting NorthernMolecular biologyClqNucleotide sequenceCloningFEBS Letters
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Monoclonal antibodies against components of the classical pathway of complement.

1989

Activation of the classical pathway of complement involves several binding and enzymatic cleavage processes. Binding and enzymatic activation results in the appearance of new structures in the individual components. This report describes the different activation steps for C1q, C1r, C1s, C4 and C2 and summarizes monoclonal antibodies reported so far which recognize either conserved epitopes or activation-dependent epitopes with particular emphasis on neoepitopes occurring during the activation cascade.

medicine.drug_classComplement Activating EnzymesImmunologyComplement C3-C5 ConvertasesComplement C3-C5 ConvertasesMonoclonal antibodyEpitopeClassical complement pathwayEpitopesComplement C1medicineComplement Pathway ClassicalComplement C1qComplement ActivationComplement component 2biologyChemistryComplement C1qAntibodies MonoclonalComplement C4HematologyComplement System ProteinsComplement C2Complement systemBiochemistrybiology.proteinAntibodyComplement and inflammation
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C1q-bearing immune complexes detected by a monoclonal antibody to human C1q in rheumatoid arthritis sera and synovial fluids

1991

Using a monoclonal antibody directed against the C-chain of human C1q, we detected C1q-bearing immune complexes (IC) in sera and synovial fluids of rheumatoid arthritis (RA) patients. In a sandwich-ELISA, C1q-bearing IC were captured by the solid-phase monoclonal antibody and then detected with peroxidase-labeled F(ab')2-antibodies to either human IgG or IgM. The results of this assay were compared to an ELISA-modification of the C1q-solid-phase binding assay (C1q-SPBA). C1q-bearing IC were detected in 81.1% of RA-sera and the 65.2% of RA-synovial fluids. IgG as well as IgM was present in 72.6% of the sera and 70% of the synovial fluids which were positive in both assays. Most RA sera that …

medicine.drug_classImmunologyEnzyme-Linked Immunosorbent Assaychemical and pharmacologic phenomenaAntigen-Antibody ComplexMonoclonal antibodyComplement Hemolytic Activity AssayArthritis RheumatoidImmunoglobulin Fab FragmentsClassical complement pathwayImmune systemRheumatologyimmune system diseasesOsteoarthritisSynovial FluidmedicineHumansImmunology and AllergySynovial fluidskin and connective tissue diseasesbiologybusiness.industryComplement C1qAntibodies Monoclonalmedicine.diseaseImmune complexImmunoglobulin MImmunoglobulin GRheumatoid arthritisMonoclonalImmunologybiology.proteinAntibodybusinessRheumatology International
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Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium.

2008

This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected, because deposits of C1q are usually observed in pathologic conditions and are associated with complement activation. In the case of DECs, we failed to detect immunoglobulins and C4 co-localized with C1q on the cell surface. Surprisingly, DECs expressed mRNA for the three chains of C1q and secreted detectable level of this component in serum-free medium. The ability to synthesize C1q is acquired by DECs during pregnancy and is not shared by…

medicine.medical_specialtyC1q; Trophoblast; Endothelial cells; GlycosaminoglycansEndotheliumBlood VesselEndothelial cellsCellImmunologychemical and pharmacologic phenomenaBiologyurologic and male genital diseasesArticleEndothelial cellimmune system diseasesPregnancyInternal medicineparasitic diseasesmedicineCell AdhesionDeciduaHumansReceptorCell adhesionskin and connective tissue diseasesMolecular BiologyC1qGlycosaminoglycansC1q; Endothelial cells; Glycosaminoglycans; Trophoblast; Blood Vessels; Cell Adhesion; Complement C1q; Decidua; Endothelial Cells; Female; Humans; Membrane Glycoproteins; Pregnancy; Receptors Complement; Trophoblasts; Molecular Biology; ImmunologyEndothelial CellMembrane GlycoproteinsComplement C1qDeciduaTrophoblastTrophoblastComplement systemCell biologyTrophoblastsReceptors Complementmedicine.anatomical_structureEndocrinologyGlycosaminoglycanBlood VesselsFemaleMembrane GlycoproteinIntracellularHuman
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An alternative role of C1q in cell migration and tissue remodeling: contribution to trophoblast invasion and placental development.

2010

Abstract Fetal trophoblast cells invading the decidua in the early phase of pregnancy establish complex interaction with the maternal extracellular matrix. We discovered that C1q was widely distributed in human decidual stroma in the absence of C4 and C3 and was actively synthesized by migrating extravillous trophoblasts. The cells expressed the messages for the three chains of C1q and secreted this complement component that interacted with the proteins of the decidual extracellular matrix. Solid phase-bound C1q promoted trophoblast adhesion and migration, and cell binding to C1q resulted in activation of ERK1/2 MAPKs. Ab inhibition experiments showed that the receptors for the globular hea…

medicine.medical_specialtyImmunologyCellIntegrinImmunoblottingchemical and pharmacologic phenomenaBiologyExtracellular matrixMicePre-Eclampsiaimmune system diseasesPregnancyInternal medicinemedicineCell AdhesionImmunology and AllergyAnimalsHumansImmunoprecipitationskin and connective tissue diseasesReceptorCell adhesionreproductive and urinary physiologyMicroscopy ConfocalC1q placental development.Reverse Transcriptase Polymerase Chain ReactionComplement C1qDeciduaTrophoblastPlacentationImmunohistochemistryPlacentationCell biologyTrophoblastsMice Inbred C57BLChemotaxis Leukocytemedicine.anatomical_structureEndocrinologyembryonic structuresbiology.proteinFemaleJournal of immunology (Baltimore, Md. : 1950)
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Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

1997

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in …

musculoskeletal diseasesImmunologyType II collagenArthritischemical and pharmacologic phenomenaInflammationPathology and Forensic Medicinefluids and secretionsAntigenimmune system diseasesSynovitismedicineImmunology and AllergyAnimalsskin and connective tissue diseasesAutoimmune diseaseInflammationbiologybusiness.industryArthritisComplement C1qmedicine.diseaseRatsRats Inbred LewRheumatoid arthritisImmunologybiology.proteinFemaleJointsmedicine.symptomAntibodybusinessOxidation-ReductionClinical immunology and immunopathology
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