Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Complement C4: A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium.Complement C3a: The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.Complement C1q: A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.Complement C5a: The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.Complement Activation: The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.Complement C4b: The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Complement C5: C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.Complement C3b: The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.Complement System Proteins: Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).Complement C6: A 105-kDa serum glycoprotein with significant homology to the other late complement components, C7-C9. It is a polypeptide chain cross-linked by 32 disulfide bonds. C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. It is encoded by gene C6.Complement C3c: A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.Complement C3d: A 302-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001).Complement C2: A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Complement C9: A 63-kDa serum glycoprotein encoded by gene C9. Monomeric C9 (mC9) binds the C5b-8 complex to form C5b-9 which catalyzes the polymerization of C9 forming C5b-p9 (MEMBRANE ATTACK COMPLEX) and transmembrane channels leading to lysis of the target cell. Patients with C9 deficiency suffer from recurrent bacterial infections.Receptors, Complement: Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.Complement C1s: A 77-kDa subcomponent of complement C1, encoded by gene C1S, is a SERINE PROTEASE existing as a proenzyme (homodimer) in the intact complement C1 complex. Upon the binding of COMPLEMENT C1Q to antibodies, the activated COMPLEMENT C1R cleaves C1s into two chains, A (heavy) and B (light, the serine protease), linked by disulfide bonds yielding the active C1s. The activated C1s, in turn, cleaves COMPLEMENT C2 and COMPLEMENT C4 to form C4b2a (CLASSICAL C3 CONVERTASE).Complement Membrane Attack Complex: A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.Complement C1r: A 80-kDa subcomponent of complement C1, existing as a SERINE PROTEASE proenzyme in the intact complement C1 complex. When COMPLEMENT C1Q is bound to antibodies, the changed tertiary structure causes autolytic activation of complement C1r which is cleaved into two chains, A (heavy) and B (light, the serine protease), connected by disulfide bonds. The activated C1r serine protease, in turn, activates COMPLEMENT C1S proenzyme by cleaving the Arg426-Ile427 bond. No fragment is released when either C1r or C1s is cleaved.Complement Inactivator Proteins: Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.Complement C7: A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.Complement C3-C5 Convertases: Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.Complement Factor B: A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.Complement Pathway, Alternative: Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement Pathway, Classical: Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement C8: A 150-kDa serum glycoprotein composed of three subunits with each encoded by a different gene (C8A; C8B; and C8G). This heterotrimer contains a disulfide-linked C8alpha-C8gamma heterodimer and a noncovalently associated C8beta chain. C8 is the next component to bind the C5-7 complex forming C5b-8 that binds COMPLEMENT C9 and acts as a catalyst in the polymerization of C9.Complement C1: The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.Receptors, Complement 3b: Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.Complement Factor H: An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).Complement C5b: The larger fragment generated from the cleavage of C5 by C5 CONVERTASE that yields COMPLEMENT C5A and C5b (beta chain + alpha' chain, the residual alpha chain, bound by disulfide bond). C5b remains bound to the membrane and initiates the spontaneous assembly of the late complement components to form C5b-8-poly-C9, the MEMBRANE ATTACK COMPLEX.Complement C2a: The COOH-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S. It is a SERINE PROTEASE. C2a combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Receptor, Anaphylatoxin C5a: A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.Complement Activating Enzymes: Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.Complement Inactivating Agents: Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.Complement Hemolytic Activity Assay: A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Receptors, Complement 3d: Molecular sites on or in B-lymphocytes, follicular dendritic cells, lymphoid cells, and epithelial cells that recognize and combine with COMPLEMENT C3D. Human complement receptor 2 (CR2) serves as a receptor for both C3dg and the gp350/220 glycoprotein of HERPESVIRUS 4, HUMAN, and binds the monoclonal antibody OKB7, which blocks binding of both ligands to the receptor.Anaphylatoxins: Serum peptides derived from certain cleaved COMPLEMENT PROTEINS during COMPLEMENT ACTIVATION. They induce smooth MUSCLE CONTRACTION; mast cell HISTAMINE RELEASE; PLATELET AGGREGATION; and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from the strongest to the weakest is C5a, C3a, C4a, and C5a des-arginine.Complement Fixation Tests: Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.Complement Factor D: A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.Complement Factor I: A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.Complement C4b-Binding Protein: A serum protein that regulates the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It binds as a cofactor to COMPLEMENT FACTOR I which then hydrolyzes the COMPLEMENT C4B in the CLASSICAL PATHWAY C3 CONVERTASE (C4bC2a).Complement C3b Inactivator Proteins: Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.Antigens, CD55: GPI-linked membrane proteins broadly distributed among hematopoietic and non-hematopoietic cells. CD55 prevents the assembly of C3 CONVERTASE or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.Complement C3-C5 Convertases, Classical Pathway: Important enzymes in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Complement C2b: The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.Antigens, CD59: Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)Cobra Venoms: Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Steroid 21-Hydroxylase: An adrenal microsomal cytochrome P450 enzyme that catalyzes the 21-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP21 gene, converts progesterones to precursors of adrenal steroid hormones (CORTICOSTERONE; HYDROCORTISONE). Defects in CYP21 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Complement C3-C5 Convertases, Alternative Pathway: Important enzymes in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. They cleave COMPLEMENT C3 and COMPLEMENT C5.Complement C1 Inhibitor Protein: An endogenous 105-kDa plasma glycoprotein produced primarily by the LIVER and MONOCYTES. It inhibits a broad spectrum of proteases, including the COMPLEMENT C1R and the COMPLEMENT C1S proteases of the CLASSICAL COMPLEMENT PATHWAY, and the MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. C1-INH-deficient individuals suffer from HEREDITARY ANGIOEDEMA TYPES I AND II.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Complement C3 Convertase, Alternative Pathway: A serine protease that is the complex of COMPLEMENT C3B and COMPLEMENT FACTOR BB. It cleaves multiple COMPLEMENT C3 into COMPLEMENT C3A (anaphylatoxin) and COMPLEMENT C3B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY.Complement C5 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 5 into COMPLEMENT 5A (anaphylatoxin) and COMPLEMENT 5B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of CLASSICAL PATHWAY C3 CONVERTASE (C4b2a) with an additional COMPLEMENT C3B, or C4b2a3b.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Complement C3 Convertase, Classical Pathway: A serine protease that cleaves multiple COMPLEMENT 3 into COMPLEMENT 3A (anaphylatoxin) and COMPLEMENT 3B in the CLASSICAL COMPLEMENT ACTIVATION PATHWAY. It is a complex of COMPLEMENT 4B and COMPLEMENT 2A (C4b2a).Antigens, CD46: A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.Opsonin Proteins: Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Lupus Erythematosus, Systemic: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.Complement C5 Convertase, Alternative Pathway: A serine protease that cleaves multiple COMPLEMENT C5 into COMPLEMENT C5A (anaphylatoxin) and COMPLEMENT C5B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. It is the complex of ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) with an additional COMPLEMENT C3B, or C3bBb3b.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Cortisone Reductase: An enzyme that catalyzes the interconversion of a ketone and hydroxy group at C-20 of cortisone and other 17,20,21-trihydroxy steroids. EC 18.104.22.168.Properdin: A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.Complement C5a, des-Arginine: A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).Mice, Inbred C57BLMacrophage-1 Antigen: An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Leukemoid Reaction: A peripheral blood picture resembling that of leukemia or indistinguishable from it on the basis of morphologic appearance alone. (Dorland, 27th ed)Serum: The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.Guanine Nucleotide Dissociation Inhibitors: Protein factors that inhibit the dissociation of GDP from GTP-BINDING PROTEINS.Immunoglobulin M: A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.Schistosoma: A genus of trematode flukes belonging to the family Schistosomatidae. There are over a dozen species. These parasites are found in man and other mammals. Snails are the intermediate hosts.Genetic Complementation Test: A test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Guanidinoacetate N-Methyltransferase: This enzyme catalyzes the last step of CREATINE biosynthesis by catalyzing the METHYLATION of guanidinoacetate to CREATINE.Arteriolosclerosis: Thickening of the walls of small ARTERIES or ARTERIOLES due to cell proliferation or HYALINE deposition.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Cell Line: Established cell cultures that have the potential to propagate indefinitely.Immunity, Innate: The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Cloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Monilethrix: Rare autosomal dominant disorder of the hair shaft. The clinical features of the disease include HYPOTRICHOSIS, dry, and/or brittle hair, with varying degrees of ALOPECIA. Mutations in the hair-specific keratin genes KRTHB1, KRTHB3, or KRTHB6 are associated with monilethrix. Autosomal recessive monilethrix with limited HYPOTRICHOSIS are also known. Mutations in Dsg4, Liph, and P2ry5 protein genes are associated with the recessive form of monilethrix.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Blood Bactericidal Activity: The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.Antigens, CD: Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Mannose-Binding Lectin: A specific mannose-binding member of the collectin family of lectins. It binds to carbohydrate groups on invading pathogens and plays a key role in the MANNOSE-BINDING LECTIN COMPLEMENT PATHWAY.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).Recombinant Proteins: Proteins prepared by recombinant DNA technology.Complement C3 Nephritic Factor: An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Immunoglobulins: Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.Haptoglobins: Plasma glycoproteins that form a stable complex with hemoglobin to aid the recycling of heme iron. They are encoded in man by a gene on the short arm of chromosome 16.DNA: A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).Surface Plasmon Resonance: A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.Peptides, Cyclic: Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).Lupus Nephritis: Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).Antibodies, Antinuclear: Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Cosmids: Plasmids containing at least one cos (cohesive-end site) of PHAGE LAMBDA. They are used as cloning vehicles.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Bacterial Proteins: Proteins found in any species of bacterium.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Mannose-Binding Protein-Associated Serine Proteases: Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.Adrenal Hyperplasia, Congenital: A group of inherited disorders of the ADRENAL GLANDS, caused by enzyme defects in the synthesis of cortisol (HYDROCORTISONE) and/or ALDOSTERONE leading to accumulation of precursors for ANDROGENS. Depending on the hormone imbalance, congenital adrenal hyperplasia can be classified as salt-wasting, hypertensive, virilizing, or feminizing. Defects in STEROID 21-HYDROXYLASE; STEROID 11-BETA-HYDROXYLASE; STEROID 17-ALPHA-HYDROXYLASE; 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES); TESTOSTERONE 5-ALPHA-REDUCTASE; or steroidogenic acute regulatory protein; among others, underlie these disorders.Species Specificity: The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.Homozygote: An individual in which both alleles at a given locus are identical.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system.ZymosanTime Factors: Elements of limited time intervals, contributing to particular results or situations.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Gene Dosage: The number of copies of a given gene present in the cell of an organism. An increase in gene dosage (by GENE DUPLICATION for example) can result in higher levels of gene product formation. GENE DOSAGE COMPENSATION mechanisms result in adjustments to the level GENE EXPRESSION when there are changes or differences in gene dosage.Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.Microbiota: The full collection of microbes (bacteria, fungi, virus, etc.) that naturally exist within a particular biological niche such as an organism, soil, a body of water, etc.HLA Antigens: Antigens determined by leukocyte loci found on chromosome 6, the major histocompatibility loci in humans. They are polypeptides or glycoproteins found on most nucleated cells and platelets, determine tissue types for transplantation, and are associated with certain diseases.Microbial Consortia: A group of different species of microorganisms that act together as a community.Sequence Homology, Nucleic Acid: The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. Sequence homology is an indication of the genetic relatedness of different organisms and gene function.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.Molecular Weight: The sum of the weight of all the atoms in a molecule.Kinetics: The rate dynamics in chemical or physical systems.Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.Exons: The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.Batrachoidiformes: An order of bottom fishes with short, small, spinous dorsal fins. It is comprised of one family (Batrachoididae) and about 70 species.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.Antimitotic Agents: Agents that arrest cells in MITOSIS, most notably TUBULIN MODULATORS.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Sweat: The fluid excreted by the SWEAT GLANDS. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products.Collectins: A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.Restriction Mapping: Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.Genes: A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Lipopolysaccharides: Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)Protein PrecursorsSteroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.Blotting, Northern: Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.DNA, Complementary: Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.Blotting, Southern: A method (first developed by E.M. Southern) for detection of DNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Macular Degeneration: Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization: A mass spectrometric technique that is used for the analysis of large biomolecules. Analyte molecules are embedded in an excess matrix of small organic molecules that show a high resonant absorption at the laser wavelength used. The matrix absorbs the laser energy, thus inducing a soft disintegration of the sample-matrix mixture into free (gas phase) matrix and analyte molecules and molecular ions. In general, only molecular ions of the analyte molecules are produced, and almost no fragmentation occurs. This makes the method well suited for molecular weight determinations and mixture analysis.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Pedigree: The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Polymorphism, Restriction Fragment Length: Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Immune Adherence Reaction: A method for the detection of very small quantities of antibody in which the antigen-antibody-complement complex adheres to indicator cells, usually primate erythrocytes or nonprimate blood platelets. The reaction is dependent on the number of bound C3 molecules on the C3b receptor sites of the indicator cell.Mice, Inbred DBAEscherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.Interleukin-1 Receptor Accessory Protein: A protein that takes part in the formation of active interleukin-1 receptor complex. It binds specifically to INTERLEUKIN-1 and the INTERLEUKIN-1 RECEPTOR TYPE I at the cell surface to form a heterotrimeric complex that brings its cytoplasmic domain into contact with the cytoplasm domain of the TYPE-I INTERLEUKIN-1 RECEPTOR. Activation of intracellular signal transduction pathways from the receptor is believed to be driven by this form of cytoplasmic interaction.Sugar AcidsTransfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Mass Behavior: Collective behavior of an aggregate of individuals giving the appearance of unity of attitude, feeling, and motivation.Arthritis, Rheumatoid: A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.Antibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Proteomics: The systematic study of the complete complement of proteins (PROTEOME) of organisms.Fluorescent Antibody Technique: Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.Interleukin-6: A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Gene Library: A large collection of DNA fragments cloned (CLONING, MOLECULAR) from a given organism, tissue, organ, or cell type. It may contain complete genomic sequences (GENOMIC LIBRARY) or complementary DNA sequences, the latter being formed from messenger RNA and lacking intron sequences.Sodium Cholate: A trihydroxy bile salt that is used as a digestive aid in dietary supplements. It is used in culture media and in conjunction with PAPAIN and PANCREATIN.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.HMGA1a Protein: An 11-kDa AT-hook motif-containing (AT-HOOK MOTIFS) protein that binds to the minor grove of AT-rich regions of DNA. It is the full-length product of the alternatively-spliced HMGA1 gene and may function as an architectural chromatin binding protein that is involved in transcriptional regulation.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
Complement component C8gamma is expressed in human fetal and adult kidney independent of C8alpha. (1/110)Human complement component C8gamma is an unusual complement factor since it shows no homology to other complement proteins but is a member of the lipocalin superfamily. So far, it has been found exclusively in plasma, covalently linked to C8alpha by disulfide bridging. We have used dot blot and Northern blot analyses of a large number of different human tissues to survey systematically the expression pattern of C8gamma. Our experiments clearly showed that besides in liver, this gene is also expressed in fetal and adult kidney. Renal expression of C8gamma is not dependent on C8alpha expression, since we could not detect C8alpha expression in kidney. Thus its physiological function is not restricted to a specific action in association with complement components. As a prerequisite for further characterization of the structure and binding activities of the uncomplexed C8gamma, we have expressed the encoding cDNA in Escherichia coli. To increase the probability for proper folding of the characteristic intramolecular disulfide bridge the recombinant protein was produced by secretion to the periplasm. (+info)
Increased ion permeability of planar lipid bilayer membranes after treatment with the C5b-9 cytolytic attack mechanism of complement. (2/110)The ion permeability of planar lipid bilayers, as measured electrically, was found to increase modestly upon treatment with purified complement complex C5b,6 and complement components C7 and C8. The subsequent addition C9 greatly amplified this change. No permeability changes occurred when components were added individually to the membrane, or when they were used in paired combinations, or when C5b, C7, C8, and C9 were admixed prior to addition. Thus, there is a significant parallel between the permeability changes induced in the model membrane and damage produced in biological membranes by the C5b-9 complement attack sequence. The efficiency of membrane action by C5b-9 was critically dependent on the order in whcih components were added to the membrane. There were also differences in the electrical properties of membranes treated with C5b-8 and C5b-9, though in both cases the enhanced bilayer permeability is best attributed to the formation of trans-membrane channels. Collectively, the data are consistent with the hypothesis that the mechanism of membrane action by complement involves the production of a stable channel across the lipid bilayer, resulting in cell death by colloid-osmotic lysis. (+info)
The role of Fcgamma receptor polymorphisms and C3 in the immune defence against Neisseria meningitidis in complement-deficient individuals. (3/110)Individuals with either a late (C5-9) complement component deficiency (LCCD) or properdin deficiency are at increased risk to develop meningococcal disease, often due to serogroups W135 and Y. Anti-meningococcal defence in both LCCD persons and properdin-deficient individuals without bactericidal antibodies depends mainly on phagocytosis. Three types of opsonin receptors are involved in phagocytosis by polymorphonuclear cells (PMN). These represent the polymorphic FcgammaRIIa (CD32) and FcgammaRIIIb (CD16b) receptors, and the C3 receptor CR3 (CD11b/CD18). When the distribution of FcgammaRIIa and FcgammaRIIIb allotypes was assessed in 15 LCCD and in 15 properdin-deficient patients with/without previous meningococcal disease, we found the combination of FcgammaRIIa-R/R131 with FcgammaRIIIb-NA2/NA2 allotypes to be associated with previous meningococcal disease (odds ratio 13.9, Fisher's test P = 0.036). No such relation was observed in the properdin-deficient patients. The importance of FcgammaRIIa allotypes was also demonstrated using in vitro phagocytosis assays. PMN from FcgammaRIIa-R/R131 homozygous donors internalized IgG2 opsonized meningococci W135 significantly (P < 0.05) less than PMN from FcgammaRIIa-H/H131 donors. When properdin-deficient serum was tested, it was observed that reconstitution with properdin resulted in enhanced PMN phagocytosis of the W135 meningococci (P = 0.001). This enhanced phagocytosis was parallelled by an increase in C3 deposition onto the opsonized meningococci W135 (r = 0.6568, P = 0. 01). We conclude that the occurrence of meningococcal disease in LCCD patients is associated with certain FcgammaR allotypes. Properdin-deficient individuals are susceptible to meningococcal disease because of an insufficient C3 deposition on the surface of meningococci, resulting in insufficient phagocytosis. (+info)
Free radicals upregulate complement expression in rabbit isolated heart. (4/110)Both free radicals and complement activation can injure tissue. Our study determined whether free radicals alter complement production by the myocardium. Isolated hearts from New Zealand White rabbits were perfused on a Langendorff apparatus and exposed to xanthine (X; 100 microM) plus xanthine oxidase (XO; 8 mU/ml) (X/XO). The free radical-generating system significantly (P < 0.05) increased C1q and also increased C1r, C3, C8, and C9 transcription compared with controls. Immunohistological examination revealed augmented membrane attack complex deposition on X/XO-treated tissue. X/XO-treated hearts also exhibited significant (P < 0.05) increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in left-ventricular developed pressure. N-(2-mercaptopropionyl)-glycine (3 mM), in conjunction with the superoxide dismutase mimetic SC-52608 (100 microM), significantly (P < 0.05) reduced the upregulation of C1q, C1r, C3, C8, and C9 mRNA expression elicited by X/XO. The antioxidants also ameliorated the deterioration in function caused by X/XO. Local complement activation may represent a mechanism by which free radicals mediate tissue injury. (+info)
CD59 protects rat kidney from complement mediated injury in collaboration with crry. (5/110)BACKGROUND: As previously reported, the membrane-bound complement regulator at the C3 level (Crry/p65) is important in maintaining normal integrity of the kidney in rats. However, the role of a complement regulator at the C8/9 level (CD59) is not clear, especially when activation of complement occurs at the C3 level. The aim of this work was to elucidate the in vivo role of CD59 under C3 activating conditions. METHODS: Two monoclonal antibodies, 5I2 and 6D1, were used to suppress the function of Crry and CD59, respectively. In order to activate alternative the pathway of complement, the left kidney was perfused with 5I2 and/or 6D1 and was recirculated. RESULTS: In the kidneys perfused with 5I2 alone, deposition of C3 and membrane attack complex (MAC) was observed in the peritubular capillaries, vasa recta, and tubular basement membranes. Cast formation, tubular dilation and degeneration, and cellular infiltration were observed at days 1 and 4, and they recovered by day 7. Further suppression of CD59 by 6D1 significantly enhanced the deposition of MAC and worsened the already exacerbated tubulointerstitial injury. These effects of 6D1 were dose dependent. Perfusion with 6D1 alone did not induce histologic damage or MAC deposition in the tubulointerstitium. CONCLUSIONS: In rats, CD59 maintains normal integrity of the kidney in collaboration with Crry in rats against complement-mediated damage in vivo. (+info)
Hypochlorite-induced alterations to canine serum complement. (6/110)Changes in the concentration of the components of complement produced by NaOC1 both in vitro and in vivo are recorded. C1, C4 and C7 are particularly sensitive to this oxidizing agent, although all components decrease at high concentrations of NaOC1. Following oxidation, complement componenets return rapidly to normal. Data are presented to indicate that part of this repair mechanism is due to the action of reducing agents such as ascorbic acid and part is due to the synthesis of the individual components. The unique sensitivity of complement components to oxidation make this treatment of potential value in suppressing the inflammatory response. (+info)
Novel mechanism of antibody-independent complement neutralization of herpes simplex virus type 1. (7/110)The envelope surface glycoprotein C (gC) of HSV-1 interferes with the complement cascade by binding C3 and activation products C3b, iC3b, and C3c, and by blocking the interaction of C5 and properdin with C3b. Wild-type HSV-1 is resistant to Ab-independent complement neutralization; however, HSV-1 mutant virus lacking gC is highly susceptible to complement resulting in > or =100-fold reduction in virus titer. We evaluated the mechanisms by which complement inhibits HSV-1 gC null virus to better understand how gC protects against complement-mediated neutralization. C8-depleted serum prepared from an HSV-1 and -2 Ab-negative donor neutralized gC null virus comparable to complement-intact serum, indicating that C8 and terminal lytic activity are not required. In contrast, C5-depleted serum from the same donor failed to neutralize gC null virus, supporting a requirement for C5. EDTA-treated serum did not neutralize gC null virus, indicating that complement activation is required. Factor D-depleted and C6-depleted sera neutralized virus, suggesting that the alternative complement pathway and complement components beyond C5 are not required. Complement did not aggregate virus or block attachment to cells. However, complement inhibited infection before early viral gene expression, indicating that complement affects one or more of the following steps in virus replication: virus entry, uncoating, DNA transport to the nucleus, or immediate early gene expression. Therefore, in the absence of gC, HSV-1 is readily inhibited by complement by a C5-dependent mechanism that does not require viral lysis, aggregation, or blocking virus attachment. (+info)
Human complement protein C8 gamma. (8/110)Human C8 gamma is a 22 kDa subunit of complement component C8, which is one of five components (C5b, C6, C7, C8, C9) that interact to form the cytolytic membrane attack complex (MAC) of complement. C8 contains three nonidentical subunits (alpha, beta, gamma) that are products of different genes. These subunits are arranged asymmetrically to form a disulfide-linked C8 alpha-gamma dimer that is noncovalently associated with C8 beta. C8 alpha and C8 beta are homologous to C6, C7 and C9 and together these proteins comprise what is referred to as the 'MAC protein family'. By comparison, C8 gamma is distinct in that it belongs to the lipocalin family of small, secreted proteins which have the common ability to bind small hydrophobic ligands. While specific roles have been identified for C8 alpha and C8 beta in the formation and function of the MAC, a function for C8 gamma and the identity of its ligand are unknown. This review summarizes the current status of C8 gamma structure and function and the progress made from efforts to determine its role in the complement system. (+info)
... proteins of the complement system (C6, C7, C8α, C8β and C9) and perforin (PF). Members of this protein family are pore-forming ... "Identity of the segment of human complement C8 recognized by complement regulatory protein CD59". J. Biol. Chem. 270 (34): ... Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex. C6, C7 and C8β appear to be ... The binding site on C8α is known, however, the precise role of C8γ in the MAC remains to be understood. Deficiency of C9, or ...
Peitsch MC, Tschopp J, Jenne DE, Haefliger JA (1991). "Structural and functional characterization of complement C8 gamma, a ... complement component C8 gamma chain; crustacyanin; epididymal-retinoic acid binding protein (E-RABP); insectacyanin; odorant ...
Figure created in Pymol Complement C8 at the US National Library of Medicine Medical Subject Headings (MeSH) The crystal ... C8 is a heterotrimer; it consists of three different subunits. These are called C8 alpha, beta and gamma chains, encoded by the ... Complement component 8 is a protein involved in the complement system. It is part of the membrane attack complex (MAC). A ... hereditary deficiency of C8 can result in increased susceptibility to Neisseria infections, such as meningitis and gonorrhea. ...
... the four genes for complement C8 gamma chain, prostaglandin-D-synthase, oncogene-24p3, and progestagen-associated endometrial ...
Outline of immunology
C6 C7 C8 C9 Complement pathway inhibitors C1-inhibitor - Classical, Lectin, Alternate Decay-accelerating factor (CD59) - ... system Complement system Classical complement pathway Mannan-binding lectin pathway Alternate complement pathway Complement ... Secreted PRRs Complement system (see complement proteins section) Collectins Mannan-binding lectin (MBL) Surfactant protein A ( ... Complement receptor CR1 (CD35) CR2 (CD21) CR3 - Heterodimer: CD11b / CD18 CR4 - Heterodimer: CD11c / CD18 CRIg (Complement ...
Hadders, M. A.; Beringer, D. X.; Gros, P. (2007). "Structure of C8 -MACPF Reveals Mechanism of Membrane Attack in Complement ... This protein is part of the oldest part of the immune system that is present in the human body, the complement system. Using ... Among his findings are the molecular mechanisms that underlie key steps in the human immune defense by the complement system, ... such as the mode of action of complement component 3 and component 8. Other research in his lab has focussed on the adhesion of ...
Complement component 5
"Evidence that C5b recognizes and mediates C8 incorporation into the cytolytic complex of complement". J. Immunol. 139 (6): 1960 ... Complement component 5 is involved in the complement system. It is cleaved into C5a and C5b: C5a plays an important role in ... Complement component 5 is the fifth component of complement, which plays an important role in inflammatory and cell killing ... 2008). "Structure of and influence of a tick complement inhibitor on human complement component 5". Nat Immunol. 9 (7): 753-60 ...
Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... When complement activation leads to deposition of C5b678 on host cells, CD59 can prevent C9 from polymerizing and forming the ... 1992). "Complement regulatory proteins at the feto-maternal interface during human placental development: distribution of CD59 ... Bohana-Kashtan O, Ziporen L, Donin N, Kraus S, Fishelson Z (July 2004). "Cell signals transduced by complement". Mol. Immunol. ...
Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ...
Terminal complement pathway deficiency
... and C8. (While C9 is part of the MAC, and deficiencies have been identified, it is not required for cell lysis.) People with ... Terminal complement pathway deficiency is a genetic condition affecting the complement membrane attack complex (MAC). It ... Initial complement tests often include C3 and C4, but not C5 through C9. Instead, the CH50 result may play a role in diagnosis ... Suspect terminal complement pathway deficiency with patients who have more than one episode of Neisseria infection. ...
Complement membrane attack complex
C8 is a complex made of the two proteins C8-beta and C8 alpha-gamma. C8 alpha-gamma has the hydrophobic area that inserts into ... MAC is composed of a complex of four complement proteins (C5b, C6, C7, and C8) that bind to the outer surface of the plasma ... two regulators of complement. The membrane attack complex is initiated when the complement protein C5 convertase cleaves C5 ... Another complement protein, C6, binds to C5b. The C5bC6 complex is bound by C7. This junction alters the configuration of the ...
The C5b then recruits and assembles C6, C7, C8 and multiple C9 molecules to assemble the membrane attack complex. This creates ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway ... The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells ...
Alternative complement pathway
C5b binds sequentially to C6, C7, C8 and then to multiple molecules of C9 to form membrane attack complex. Since C3b is free ... Inhibition of the alternative complement pathway by antisense oligonucleotides targeting complement factor B improves lupus ... cells from complement-mediated damage. CFHR5 (Complement Factor H-Related protein 5) is able to bind to act as a cofactor for ... there are several different kinds of regulatory proteins that disrupt the complement activation process: Complement Receptor 1 ...
... three proteins involved in the complement system (part of the immune system) Cervical spinal nerve 8 in human anatomy An octyl- ... C8; PFOA), a ubiquitous chemical used in the production of PTFE (Teflon) Citroën C8, a brand of minivan LSWR C8 class, a London ... C8, C08, C.VIII or C-8 may refer to: AEG C.VIII, a World War I German armed reconnaissance aircraft AGO C.VIII, a World War I ... IATA code HMS C8, a C-class submarine of the Royal Navy USS Raleigh (C-8), a protected cruiser of the United States Navy Code ...
List of MeSH codes (D12.776.124)
... complement c6 MeSH D12.776.124.486.274.650 -- complement c7 MeSH D12.776.124.486.274.750 -- complement c8 MeSH D12.776.124.486. ... complement c4a MeSH D12.776.124.486.274.024.270 -- complement c5a MeSH D12.776.124.486.274.024.270.255 -- complement c5a, des- ... complement c1r MeSH D12.776.124.486.274.050.290 -- complement c1s MeSH D12.776.124.486.274.150 -- complement c2 MeSH D12.776. ... complement c2b MeSH D12.776.124.486.274.250 -- complement c3 MeSH D12.776.124.486.274.250.250 -- complement c3a MeSH D12.776. ...
Complement component 9
C7 and C8. Lint TF, Zeitz HJ, Gewurz H (November 1980). "Inherited deficiency of the ninth component of complement in man". J. ... Complement component 9 (C9) is a protein involved in the complement system, which is part of the innate immune system. C9 is a ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ... There are 10-16 molecules of C9 in a single membrane attack complex (MAC), along with one of each of the complement components ...
Classical complement pathway
Subsequent interactions between C5b and other terminal components C6, C7, C8, and C9 form the membrane attack complex or the ... Alternative complement pathway - another complement system pathway Lectin pathway - another complement system pathway Noris, ... The classical complement pathway is one of three pathways which activate the complement system, which is part of the immune ... Activation of the complement pathway through the classical, lectin or alternative complement pathway is followed by a cascade ...
Autoimmune hemolytic anemia
Cases may also arise with complement alone or with IgA, IgM or a combination of these three antibody classes and complement. ... C8, C9) either can form the membrane attack complex (MAC) or can bind the antibody, aiding phagocytosis by macrophages (C3b). ... Antibodies are produced against the RBCs, which leads to complement activation. Complement fragments, such as C3a, C4a and C5a ... IgM is a potent activator of the classical complement pathway, thus, AIHA involving IgM is characterized by complement mediated ...
For decades, the two complemented each other within the same integrated factory. Until 1855, the works belonged to the Treasury ...
The C1 complement complex binds to these antibodies resulting in its activation via cross proteolysis. This activated C1 ... C5b associates with C6, C7, C8, and C9, all of which form a complex that results in a pore through the pathogen's membrane. ... C3b is the larger of two elements formed by the cleavage of complement component 3, and is considered an important part of the ... The key to the success of the complement system in clearing antigens is regulating the effects of C3b to pathogens alone and ...
Ștefan Vodă District
Forests of the district are complemented by tree species such as oak, ash, hornbeam, linden, maple, walnut and others. From ...
Forests occupy 19.3% of the district and are complemented by oak, ash, lime, hornbeam, acacia and others. Plants include: ...
Pattern recognition receptor
C5b recruits C6, C7, C8 and multiple C9s. C5, C6, C7, C8 and C9 form the membrane attack complex (MAC). This is another large ... Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... Once bound to the ligands MBL and Ficolin oligomers recruit MASP1 and MASP2 and initiate the lectin pathway of complement ... "/"self turned nonself" type pathogen pattern are also identified and destroyed (e.g. by complement fixation or other cytotoxic ...
Constantin S. Nicolăescu-Plopșor
The ethnographic overview of Oltenia is complemented by a depiction of the region's southern parts, through an account of ...
Spoleto Festival USA
p. C8. Retrieved May 24, 2013. Jerry R. Sanders (Sep 28, 1976). "Stern to Head Spoleto". Charleston News & Courier. p. 1A. ... Piccolo Spoleto is "the perfect complement to the international scope of its parent festival and its 700 events in 17 days ...
HMS Temeraire (1798)
Essex Record Office: D/DGu/C8. as cited in Willis. The Fighting Temeraire. p. 192. Adkin, Mark (2007). The Trafalgar Companion ... Vice-Admiral Mitchell was granted extraordinary powers regarding the death sentence and Temeraire's marine complement was ... and provided men from her sailor and marine complement to crew batteries and gunboats. Men from Temeraire were heavily involved ...
Egan LJ et. al. (1994) Hereditary deficiency of the seventh component of complement and recurrent meningococcal infection: investigations of an Irish family using a novel haemolytic screening assay for complement activity and C7 M/N allotyping.. [^] ...
Gamma motoneurons regulate how sensitive the stretch reflex is by tightening or relaxing the fibers within the spindle. There are several theories as to what may trigger gamma motoneurons to increase the reflexs sensitivity. For example, alpha-gamma co-activation might keep the spindles taut when a muscle is contracted, preserving stretch reflex sensitivity even as the muscle fibers become shorter. Otherwise the spindles would become slack and the reflex would cease to function. ...
Alloantibodies in pre-sensitized transplant candidates deposit complement membrane attack complexes (MAC) on graft endothelial cells (ECs), increasing risk of CD8+ T cell-mediated acute rejection. We recently showed (a) human ECs endocytose MAC into Rab5+ endosomes, creating a signaling platform that stabilizes NF-κB-inducing kinase (NIK) protein; (b) endosomal NIK activates both non-canonical NF-κB signaling to synthesize pro-IL-1β and an NLRP3 inflammasome to process and secrete active IL-1β; and (c) IL-1β activates ECs, increasing recruitment and activation of alloreactive effector memory CD4+ T (TEM) cells. Here, we report IFN-γ priming induced nuclear expression of IL-15/IL-15Rα complexes in cultured human ECs and that MAC-induced IL-1β stimulated translocation of IL-15/IL-15Rα complexes to the EC surface in a canonical NF-κB-dependent process, where IL-15/IL-15Rα transpresentation increased activation and maturation of alloreactive CD8+ TEM. Blocking NLRP3 inflammasome assembly, ...
Herein reported is the case of a 15-year-old female without a relevant medical history, who developed severe headaches, speech problems, dizziness, weakness, inability to walk, depressed consciousness, confusion, amnesia and vomiting, 14 days after receiving her first qHPV vaccine injection. After the second vaccine booster, her symptoms worsened and she expired 15 days later. Autopsy revealed cerebral oedema and cerebellar herniation indicative of a focally disrupted blood-brain barrier.. There was no evidence of an active brain infection. Immunohistochemistry (IHC) examination of the brainstem, hippocampus and the cerebellum showed prominent infiltration of T-lymphocytes and macrophages in all brain areas examined. Notably, marked activation of the complement membrane attack complex (MAC) was detected in the cerebellar Purkinje cells, hippocampal neurons and portions of the brainstem. This pattern of MAC activation in the absence of an active brain infection indicates an abnormal triggering of ...
Regenesance is developing nanoparticle formulations of inhibitors of the complement membrane attack complex (MAC) for the treatment of peripheral neuropathy.
CD59, an LY-6-like protein expressed in human lymphoid cells, regulates the action of the complement membrane attack complex on...
A novel cell surface antigen has been identified on a wide range of lymphoid cells and erythrocytes. A mAb YTH 53.1 (CD59) against this antigen enhanced the lysis of human red cells and lymphocytes by homologous complement. Studies of reactive lysis using different species of C56, and of whole serum used as a source of C7-9, indicated that the inhibitory activity of the CD59 antigen is directed towards the homologous membrane attack complex. CD59 antigen was purified from human urine and erythrocyte stroma by affinity chromatography using the mAb YTH 53.1 immobilized on Sepharose, and, following transient expression of a human T cell cDNA library in COS cells, the corresponding cDNA also identified using the antibody. It was found that the CD59 antigen is a small protein (approximately 20 kD as judged by SDS-PAGE, 11.5 kD predicted from the isolated cDNA) sometimes associated with larger components (45 and 80 kD) in urine. The sequence of CD59 antigen is unlike that of other complement ...
The membrane attack complex of complement: Relation of C7 to the metastable membrane binding site of the intermediate complex...
TY - JOUR. T1 - The membrane attack complex of complement. T2 - Relation of C7 to the metastable membrane binding site of the intermediate complex C5b-7. AU - Preissner, K. T.. AU - Podack, E. R.. AU - Muller-Eberhard, H. J.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent, C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization, C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing ...
The membrane attack complex of complement: relation of C7 to the metastable membrane binding site of the intermediate complex...
Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent. C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization. C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing complexes also contained 131I label; again suggesting that C5b-7 consisted of oligomers rather than monomers. The conformation of C7 in C5b-7 and in dimeric C7 appeared similar by the following criteria. On formation of C5b-7 from C5b,6 and C7, a 20% increase in ...
Die genetische Anfälligkeit für Meningokokken-Infektionen liegt vor allem in Störungen des Komplementsystems begründet, vor allem der terminale membrane attack complex (MAC), der von C8 und C9 gebildet wird, aber auch Teile des Komplementsystems, die die Bildung des MAC steuern, können betroffen sein (C3, C5, C6, C7).. ...
Complement component C9 binds to the C5b-8 complex as the final protein of the membrane attack complex. After binding, it undergoes a conformational change and inserts itself into the cell membrane, forming transmembrane channels.
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells (PubMed:9634479, PubMed:9212048, PubMed:26841934). C9 is the pore-forming subunit of the MAC (PubMed:4055801, PubMed:26841934, PubMed:30111885).
Abcams Complement C4 ELISA Kit (ab108825) suitable for Cell culture supernatant, Saliva, Milk, Urine, Cerebral Spinal Fluid in human. Reliably quantify 0.07…
The complement system (Chap. 308) consists of a group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes that adhere to- and in some cases disrupt-the surface of invading organisms. Some of these surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes. The later, "terminal" components (C7, C8, and C9) can directly kill some bacterial invaders (notably, many of the neisseriae) by forming a membrane attack complex and disrupting the integrity of the bacterial membrane, thus causing bacteriolysis. ...
Membrane attack complex (MAC) is formed under the combined stimulation of amyloid beta (Aβ) and normal human serum (NHS), immunolabeled with a monoclonal mouse anti-human C5b-9 antibody and subsequently visualized by Cy3 (red). RPE cell nuclei are counter-stained with DAPI. Scale bars: 20 μm. See full article online. Read More ...
Constituent of the membrane attack complex (MAC) that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells.
Dr. Elias Reichel, of Tufts University School of Medicine and a founder of Hemera Biosciences, Inc., of Boston, MA, presented on a new approach to treating the dry form of age-related macula degeneration. His paper was based on the research being done by Hemera Biosciences on HMR59, a naturally occurring protein that protects retinal cells from damage by MAC (Membrane Attack Complex), that can be delivered for long-lasting activity via a gene therapy approach. ...
Complement system activation contributes to the ependymal damage induced by microbial neuraminidase -ORCA
Background In the rat brain, a single intracerebroventricular injection of neuraminidase from Clostridium perfringens induces ependymal detachment and death. This injury occurs before the infiltration of inflammatory blood cells; some reports implicate the complement system as a cause of these injuries. Here, we set out to test the role of complement. Methods The assembly of the complement membrane attack complex on the ependymal epithelium of rats injected with neuraminidase was analyzed by immunohistochemistry. Complement activation, triggered by neuraminidase, and the participation of different activation pathways were analyzed by Western blot. In vitro studies used primary cultures of ependymal cells and explants of the septal ventricular wall. In these models, ependymal cells were exposed to neuraminidase in the presence or absence of complement, and their viability was assessed by observing beating of cilia or by trypan blue staining. The role of complement in ependymal damage induced by ...
[A type of glomerulonephritis that is characterized by the accumulation of immune deposits ( COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane., A slowly progressive inflammation of the glomeruli characterized by immune complex deposits at the glomerular basement membrane, resulting in a thickened membrane, and nephrotic syndrome.]
Meningococcal infections are caused by a bacteria called Neisseria meningitidis. The most common forms of meningococcal infections include meningitis and meningococcemia . Meningococcal infections are uncommon, but can be fatal.
Complement component C8 beta chain - DrugBank
Complement component C8 beta chain. Details. Name. Complement component C8 beta chain. Synonyms. *Complement component 8 ... complement activation / complement activation, alternative pathway / complement activation, classical pathway / cytolysis / ... Haefliger JA, Tschopp J, Nardelli D, Wahli W, Kocher HP, Tosi M, Stanley KK: Complementary DNA cloning of complement C8 beta ... Dewald G, Hemmer S, Nothen MM: Human complement component C8. Molecular basis of the beta-chain polymorphism. FEBS Lett. 1994 ...https://www.drugbank.ca/polypeptides/P07358
C8B - Complement component C8 beta chain precursor - Homo sapiens (Human) - C8B gene & protein
Complement component C8 beta chainAdd BLAST. 537. Amino acid modifications. Feature key. Position(s). DescriptionActions. ... "Human complement component C8. Molecular basis of the beta-chain polymorphism.". Dewald G., Hemmer S., Noethen M.M.. FEBS Lett ... Belongs to the complement C6/C7/C8/C9 family.Curated. Keywords - Domaini. EGF-like domain, Repeat, Signal. Phylogenomic ... IPR037566 Complement_C8_beta. IPR036055 LDL_receptor-like_sf. IPR023415 LDLR_class-A_CS. IPR002172 LDrepeatLR_classA_rpt. ...https://www.uniprot.org/uniprot/P07358
RCSB PDB - 2QOS: Crystal structure of complement protein C8 in complex with a peptide containing the C8 binding site...
Crystal structure of complement protein C8gamma in complex with a peptide containing the C8gamma binding site on C8alpha: ... Crystal structure of complement protein C8 in complex with a peptide containing the C8 binding site on C8. *DOI: 10.2210/ ... Complement component C8 alpha chain A 11 Homo sapiens Mutation: C164A Gene Name(s): C8A Gene View ... Complement component 8, gamma polypeptide C 173 Homo sapiens Mutation: C40A Gene Name(s): C8G Gene View ...http://www.rcsb.org/pdb/explore/explore.do?structureId=2qos
Complement component C8, A chain
... The C8A gene encodes the alpha subunit of the complement component 8. C8 participates in the ... Genomic organization of human complement protein C8 alpha and further examination of its linkage to C8 beta. ... Merritt AD et al. (1976) Chromosome 6: linkage of the eighth component of complement (C8) to the histocompatibility region (HLA ... Evidence for two unlinked genetic loci for the eighth component of human complement (C8). ...http://moldiag.com/en/id/G0270
"Human Complement Protein C8: Crystal Structure and Analysis of Binding" by Christopher Langston Cooper
The MAC is comprised of complement proteins C5b, C6, C7, C8 and C9. The 150-kDa C8 protein consists of three non-identical ... The role of C8 within the MAC is to initiate formation of a transmembrane pore consisting of 12-18 molecules of C9. ... Human C8 is part of the membrane attack complex (MAC) that assembles on bacterial cell membranes to form a lethal pore-like ... The MAC is comprised of complement proteins C5b, C6, C7, C8 and C9. The 150-kDa C8 protein consists of three non-identical ...https://scholarcommons.sc.edu/etd/668/
KAKEN - Research Projects | Planning-Coordination Committe on Special Cancer Research (KAKENHI-PROJECT-09042003)
Publications] Kojima,T.: Genetic basis of human complement c8 α-γ deficiency. J.Immunology. 161. 3762-3766 (1998). *. Related ... Publications] Kojima, T.: Genetic basis of human complement c8 α-γ deficiency. J.Immunology. 161. 3762-3766 (1998). *. ... Publications] Kojima, T.: Genetic basis of human complement c8 alpha-gamma deficiency. J.Immunology. 161. 3762-3766 (1998). * ...https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09042003/
Complement System and Its Role in Immune Responses
The complement system is a network of more than 50 plasma proteins and receptors, which have the role of mediating innate and ... 2011) Structure of human complement C8, a precursor to membrane attack. Journal of Molecular Biology 405(2): 325-330. ... Complement activation pathways. The components of complement system can be organised into three major pathways: The classical ... 2009) Complement in human diseases: Lessons from complement deficiencies. Molecular Immunology 46(14): 2774-2783. ...http://www.els.net/WileyCDA/ElsArticle/refId-a0000508.html
34. Infections in immunodeficiency Flashcards by Eva Gonzales | Brainscape
A boy with C8 complement deficiency requires a vaccine. Which vaccine does he need? Which bacterium is he most susceptible to ... Meningococcal vaccine; Neisseria, as there is no formation of membrane attack complex (late complement deficiency). ... bacteria encapsuled species with early complement deficiencies, Neisseria with late compoment deficiencies ...https://www.brainscape.com/flashcards/34-infections-in-immunodeficiency-5336270/packs/7987181
Hypercholesterolemia, Familial, 4 disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials
Complement C8 Alpha Chain. Protein Coding. 6.96. DISEASES inferred 15 26. PDCL2 ...https://www.malacards.org/card/hypercholesterolemia_familial_4
Enzyme Explorer Key Resource: Plasma Proteins Table | Sigma-Aldrich
Includes, Albumin, Complement Products, Lipoprotein Products, Plasma Proteins, RBC Proteins and Sera and Plasma. ... Complement C8 deficient serum human. C1538. Complement C8 from human serum, 1 mg/mL in 15 mM sodium phosphate, 150 mM NaCl, pH ... Complement C9 deficient serum human C1663. Complement C9 from human serum, 1 mg/mL in 15 mM sodium phosphate, 135 mM NaCl, pH ... Complement C3 from human serum, ~95% (SDS-PAGE) lyophilized powder. C0651. Complement C3 from human serum, ,50 C3H50 units/mg ( ...https://www.sigmaaldrich.com/life-science/metabolomics/enzyme-explorer/learning-center/plasma-blood-protein/plasma-proteins-table.html
Hypercholesterolemia, Familial, 4 disease: Malacards - Research Articles, Drugs, Genes, Clinical Trials
Complement C8 Alpha Chain. Protein Coding. 6.96. DISEASES inferred 15 26. PDCL2 ...https://www.malacards.org/card/hypercholesterolemia_familial_4?showAll=True
Maria Antonietta Villa - Research Output - Italian Ministry of Health
Two types of dysfunctional eighth component of complement (C8) molecules in C8 deficiency in man. Reconstitution of normal C8 ... Functional C8 associated with human platelets. Tedesco, F., Densen, P., Villa, M. A., Presani, G., Roncelli, L. & Rosso di san ... β Chain deficiency in three patients with dysfunctional C8 molecules. Tedesco, F., Villa, M. A., Densen, P. & Sirchia, G., 1983 ... from the mixture of two abnormal C8 molecules. Tedesco, F., Densen, P., Villa, M. A., Petersen, B. H. & Sirchia, G., 1983, In ...https://moh-it.pure.elsevier.com/en/persons/maria-antonietta-villa/publications/?type=%2Fdk%2Fatira%2Fpure%2Fresearchoutput%2Fresearchoutputtypes%2Fcontributiontojournal%2Farticle
Immune System Flashcards by Lauren Schnitzen | Brainscape
Complement mediates the induction of granule release from mast cells and recruitment of inflammatory cells into the tissue ... What results from deficiencies in terminal complement C5-C8? Associated with recurrent infections ... Once activates, what is the role of the complement in a type III hypersensitivity reaction? ... Stimulates mast cells to release histamine and activates the complement pathway leading to thromboxane production ...https://www.brainscape.com/flashcards/immune-system-4582753/packs/6196692
MACPF - Wikipedia
... proteins of the complement system (C6, C7, C8α, C8β and C9) and perforin (PF). Members of this protein family are pore-forming ... "Identity of the segment of human complement C8 recognized by complement regulatory protein CD59". J. Biol. Chem. 270 (34): ... Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex. C6, C7 and C8β appear to be ... The binding site on C8α is known, however, the precise role of C8γ in the MAC remains to be understood. Deficiency of C9, or ...https://en.wikipedia.org/wiki/MACPF
Recombinant Human C8G protein (ab113121) | Abcam
Complement component 8 gamma polypeptide. *Complement component C8 gamma chain. *MGC142186. see all ... C8 is a constituent of the membrane attack complex. C8 binds to the C5B-7 complex, forming the C5B-8 complex. C5-B8 binds C9 ...https://www.abcam.com/recombinant-human-c8g-protein-ab113121.html
Lipocalin - Wikipedia
Peitsch MC, Tschopp J, Jenne DE, Haefliger JA (1991). "Structural and functional characterization of complement C8 gamma, a ... complement component C8 gamma chain; crustacyanin; epididymal-retinoic acid binding protein (E-RABP); insectacyanin; odorant ...https://en.wikipedia.org/wiki/Lipocalin
IUCr) Acta Crystallographica Section D Volume 63, Part 6, June 2007
Crystal structure of CD59: implications for molecular recognition of the complement proteins C8 and C9 in the membrane-attack ... The crystal structure of the human complement protein CD59 is presented at 2.1 Å resolution. This structure is compared with a ... previous NMR model and the binding region for C8 and C9 is mapped. ...http://journals.iucr.org/d/issues/2007/06/00/index.html
ELISA Kits, Antibodies, Pathway Inhibitors, Antibody Arrays Antibodies - Jomar Life Research
Complement C8 (2) * Copine-1 (2) * Coronin-1A (3) * Cullin-5 (1) ...https://www.jlresearch.com.au/antibodies.html?lr_species=Rabbit
Postmenopausal estrogen and progestin effects on the serum proteome | Genome Medicine | Full Text
... complement and immune response, and cell adhesion. Moreover, the changes (base 2 logarithm of 1-year-to-baseline concentration ...https://genomemedicine.biomedcentral.com/articles/10.1186/gm121
Table], What is the prevalence of primary immunodeficiency in children and young people with meningococcal disease? - Bacterial...
Hereditary complement deficiency in survivors of meningococcal disease: high prevalence of C7/C8 deficiency in Sephardic ( ... Genetic aspects of complement component C8 in Norwegian meningococcal disease patients. Scandinavian Journal of Infectious ... Complement deficiencies in patients over ten years old with meningococcal disease due to uncommon serogroups: Comment. ... Low prevalence of complement deficiencies among patients with meningococcal disease in Norway. Scandinavian Journal of ...https://www.ncbi.nlm.nih.gov/books/NBK83066/table/appendixes.app6.tu31/?report=objectonly
GSE17721 CTRL VS GARDIQUIMOD 24H BMDC UP
complement C8 gamma chain [Source:.... CARHSP1. 23589. CARHSP1. calcium regulated heat stable prot.... ...http://software.broadinstitute.org/gsea/msigdb/geneset_page.jsp?geneSetName=GSE17721_CTRL_VS_GARDIQUIMOD_24H_BMDC_UP
Transcriptomic assessment of resistance to effects of an aryl hydrocarbon receptor (AHR) agonist in embryos of Atlantic...
... complement C8 beta chain precursor, type II antifreeze protein precursor, and an unannotated gene (UnAn_22873). As seen at the ...https://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-12-263
Human Complement C7 ELISA Kit - Innovative Research
Human Complement C7 ELISA Kit is designed for detection of C7 in human plasma, serum, urine, milk, saliva, and cell culture ... 30 homology with Complements C8 and C9 (1). C7 is one of five complement proteins (C5b, C6, C7, C8, and C9)that assemble on ... Human Complement C7 ELISA Kit. Human Complement C7 ELISA Kit is designed for detection of C7 in human plasma, serum, urine, ... Human Complement Component 7 (C7) is a single-chain glycoprotein consisting of 821 amino acid residues with a molecular weight ...https://www.innov-research.com/product/human-complement-c7-elisa-kit
SMART: TSP1 domain annotation
Crystal Structure of Human Complement Component C8. 3r6b. Crystal Structure of Thrombospondin-1 TSR Domains 2 and 3. ... Crystal Structure of human Complement Component C6. 3vdj. Crystal structure of circumsporozoite protein aTSR domain, R32 native ... Complement component C6 (P13671) (SMART). OMIM:217050: C6 deficiency ; Combined C6/C7 deficiency. ... Now a number of proteins involved in the complement pathway (properdin, C6, C7, C8A, C8B, C9) [(PUBMED:2459396)] as well as ...http://smart.embl.de/smart/do_annotation.pl?DOMAIN=TSP1&START=547&END=584&E_VALUE=1.17e-1&TYPE=SMART&BLAST=WSCWSDWSACSGGHKTRHRQCNNPAPHKGGSPCSGPAS
SMART: TSP1 domain annotation
Crystal Structure of Human Complement Component C8. 3r6b. Crystal Structure of Thrombospondin-1 TSR Domains 2 and 3. ... Crystal Structure of human Complement Component C6. 3vdj. Crystal structure of circumsporozoite protein aTSR domain, R32 native ... Complement component C6 (P13671) (SMART). OMIM:217050: C6 deficiency ; Combined C6/C7 deficiency. ... Now a number of proteins involved in the complement pathway (properdin, C6, C7, C8A, C8B, C9) [(PUBMED:2459396)] as well as ...http://smart.embl.de/smart/do_annotation.pl?DOMAIN=TSP1&START=1186&END=1240&E_VALUE=1.45e-6&TYPE=SMART&BLAST=WRFGSWTPCSATCGKGTRMRYVSCRDEDGSVADESACATLPKPVAKEECSVTPCG
- C8 participates in the formation of the membrane attack complex (MAC) which disrupts bacterial walls, which mediates cell lysis. (moldiag.com)
- Human C8 is part of the membrane attack complex (MAC) that assembles on bacterial cell membranes to form a lethal pore-like structure. (sc.edu)
- The Membrane Attack Complex/Perforin (MACPF) superfamily, sometimes referred to as the MACPF/CDC superfamily, is named after a domain that is common to the membrane attack complex (MAC) proteins of the complement system (C6, C7, C8α, C8β and C9) and perforin (PF). (wikipedia.org)
- Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex. (wikipedia.org)
- 2011) Structure of human complement C8, a precursor to membrane attack. (els.net)
- C8 is a constituent of the membrane attack complex. (abcam.com)
- C7 is one of five complement proteins (C5b, C6, C7, C8, and C9)that assemble on pathogen membranes to form the lethal membrane attack complex. (innov-research.com)
- Mutations cause autosomal recessive complement C8 deficiency type 1. (moldiag.com)
- C8 deficiency in a family with xeroderma pigmentosum. (moldiag.com)
- A boy with C8 complement deficiency requires a vaccine. (brainscape.com)
- Prevalence of congenital or acquired complement deficiency in patients with sporadic meningocococcal disease. (nih.gov)
- Complement deficiency predisposes for meningitis due to nongroupable meningococci and Neisseria-related bacteria. (nih.gov)
- Systemic meningococcal infections in patients with acquired complement deficiency. (nih.gov)
- The remaining two isolates were from recurrent disease episodes (8 months apart) in a male child with deficiency of the sixth complement component, and with the exception of two single nucleotide polymorphisms, contained identical core genomes. (beds.ac.uk)
- Case 6: Deficiency of the C8 Complement Component 7. (taylorfrancis.com)
- The primary functions mediated by complement proteins include phagocytosis of foreign elements (bacteria, viruses, particles etc .), cell lysis, inflammation, solubilisation of immune complexes, apoptotic cell clearance and enhancement of humoral immune responses. (els.net)
- C5b subsequently takes the lead in formation of the terminal C5b-9 complement complex ( TCC ), ultimately resulting into cell lysis. (els.net)
- This gene encodes a cell surface glycoprotein that regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. (genetex.com)
- Complement dysregulation and deficiencies are connected to disease. (els.net)
- 2009) Complement in human diseases: Lessons from complement deficiencies. (els.net)
- Complement deficiencies in patients over ten years old with meningococcal disease due to uncommon serogroups: Comment. (nih.gov)
- Low prevalence of complement deficiencies among patients with meningococcal disease in Norway. (nih.gov)
- Prevalence of complement deficiencies in children with systemic meningococcal infections. (nih.gov)
- Complement activation pathways. (els.net)
- The components of complement system can be organised into three major pathways: The classical pathway is mainly initiated by the binding of C1q to antigen-antibody complexes, whereas the lectin pathway is triggered by binding of mannose‐binding lectin ( MBL ) or ficolins to glycosylated surfaces on microbial cell walls. (els.net)
- C3 convertases generated by all pathways are able to cleave C3 into C3a and C3b, latter of which forms additional convertases, thereby rapidly amplifying complement response. (els.net)