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).Anaplasma marginale: A species of gram-negative bacteria and causative agent of severe bovine ANAPLASMOSIS. It is the most pathogenic of the ANAPLASMA species.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.Phosphotransferases (Nitrogenous Group Acceptor): A group of enzymes that catalyzes the transfer of a phosphate group onto a nitrogenous group acceptor. EC 2.7.3.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.Phosphoenolpyruvate Sugar Phosphotransferase System: The bacterial sugar phosphotransferase system (PTS) that catalyzes the transfer of the phosphoryl group from phosphoenolpyruvate to its sugar substrates (the PTS sugars) concomitant with the translocation of these sugars across the bacterial membrane. The phosphorylation of a given sugar requires four proteins, two general proteins, Enzyme I and HPr and a pair of sugar-specific proteins designated as the Enzyme II complex. The PTS has also been implicated in the induction of synthesis of some catabolic enzyme systems required for the utilization of sugars that are not substrates of the PTS as well as the regulation of the activity of ADENYLYL CYCLASES. EC 2.7.1.-.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.Bacterial Proteins: Proteins found in any species of bacterium.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 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 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 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 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 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 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 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 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.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 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 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.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.Gene Expression Regulation, Bacterial: Any of the processes by which cytoplasmic or intercellular factors influence the differential control of gene action in bacteria.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 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 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.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: 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.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 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 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 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 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 C4a: The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A.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 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 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 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.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 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.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 C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Complement Pathway, Mannose-Binding Lectin: Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.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.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.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 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.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.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.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.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.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.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)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.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.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 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 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 C2b: The N-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S.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.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.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.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.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Lectins: Proteins that share the common characteristic of binding to carbohydrates. Some ANTIBODIES and carbohydrate-metabolizing proteins (ENZYMES) also bind to carbohydrates, however they are not considered lectins. PLANT LECTINS are carbohydrate-binding proteins that have been primarily identified by their hemagglutinating activity (HEMAGGLUTININS). However, a variety of lectins occur in animal species where they serve diverse array of functions through specific carbohydrate recognition.ZymosanBlood 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.Phthalic Anhydrides: Phthalic acid anhydrides. Can be substituted on any carbon atom. Used extensively in industry and as a reagent in the acylation of amino- and hydroxyl groups.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).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.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.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.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.Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.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.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.Sarcoptes scabiei: A species of mite that causes SCABIES in humans and sarcoptic mange in other animals. Specific variants of S. scabiei exist for humans and animals, but many have the ability to cross species and cause disease.gamma-Globulins: Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.Snake Venoms: Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.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.Forssman Antigen: A glycolipid, cross-species antigen that induces production of antisheep hemolysin. It is present on the tissue cells of many species but absent in humans. It is found in many infectious agents.Serum: The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Veillonella: A genus of gram-negative, anaerobic cocci parasitic in the mouth and in the intestinal and respiratory tracts of man and other animals.Bothrops: A genus of poisonous snakes of the VIPERIDAE family. About 50 species are known and all are found in tropical America and southern South America. Bothrops atrox is the fer-de-lance and B. jararaca is the jararaca. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p336)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.Macrophage-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.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.Mice, Inbred C57BLImmune Evasion: Methods used by pathogenic organisms to evade a host's immune system.Oxyphenbutazone: A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27)Mannans: Polysaccharides consisting of mannose units.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).Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Integrin alphaXbeta2: A major adhesion-associated heterodimer molecule expressed by MONOCYTES; GRANULOCYTES; NK CELLS; and some LYMPHOCYTES. The alpha subunit is the CD11C ANTIGEN, a surface antigen expressed on some myeloid cells. The beta subunit is the CD18 ANTIGEN.Snakes: Limbless REPTILES of the suborder Serpentes.Immune Complex Diseases: Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.Dose-Response Relationship, Immunologic: A specific immune response elicited by a specific dose of an immunologically active substance or cell in an organism, tissue, or cell.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.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.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.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.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.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.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.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Sheep: Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Hemolytic-Uremic Syndrome: A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.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.Urochordata: A subphylum of chordates intermediate between the invertebrates and the true vertebrates. It includes the Ascidians.Kaolin: The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: "high ridge"), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed)Arthropod Proteins: Proteins synthesized by organisms belonging to the phylum ARTHROPODA. Included in this heading are proteins from the subdivisions ARACHNIDA; CRUSTACEA; and HORSESHOE CRABS. Note that a separate heading for INSECT PROTEINS is listed under this heading.Antigen-Antibody Reactions: The processes triggered by interactions of ANTIBODIES with their ANTIGENS.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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Leukocytes: White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).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)Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells.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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Protein S: The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.Chemotaxis, Leukocyte: The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.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.Recombinant Proteins: Proteins prepared by recombinant DNA technology.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.Mannose: A hexose or fermentable monosaccharide and isomer of glucose from manna, the ash Fraxinus ornus and related plants. (From Grant & Hackh's Chemical Dictionary, 5th ed & Random House Unabridged Dictionary, 2d ed)Polysaccharides, Bacterial: Polysaccharides found in bacteria and in capsules thereof.Sepsis: Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.Reperfusion Injury: Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.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.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.)Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Kinetics: The rate dynamics in chemical or physical systems.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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Mice, Inbred BALB CElectrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.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.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.Immune System: The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Histocompatibility Antigens: A group of antigens that includes both the major and minor histocompatibility antigens. The former are genetically determined by the major histocompatibility complex. They determine tissue type for transplantation and cause allograft rejections. The latter are systems of allelic alloantigens that can cause weak transplant rejection.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).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.PolysaccharidesEscherichia 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.Molecular Weight: The sum of the weight of all the atoms in a molecule.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Antibodies, Bacterial: Immunoglobulins produced in a response to BACTERIAL ANTIGENS.Shock, Septic: Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.Peptide Hydrolases: Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.

Interaction of inflammatory cells and oral microorganisms. III. Modulation of rabbit polymorphonuclear leukocyte hydrolase release response to Actinomyces viscosus and Streptococcus mutans by immunoglobulins and complement. (1/3896)

In the absence of antiserum, rabbit polymorphonuclear leukocytes (PMNs) released lysosomal enzymes in response to Actinomyces viscosus (19246) but not to Streptococcus mutans (6715). Antibodies had a marked modulating influence on these reactions. PMN hydrolase release was significantly enhanced to both organisms when specific rabbit antiserum and isolated immunoglobulin G (IgG) were included in the incubations. Immune complex F(ab')2 fragments of IgG directed against S. mutans agglutinated bacteria. Immune complexes consisting of S. mutans and F(ab')2 fragments of IgG directed against this organism were not effective as bacteria-IgG complexes in stimulating PMN release. The intensity of the release response to bacteria-IgG complexes was also diminished when PMNs were preincubated with isolated Fc fragments derived from IgG. Fresh serum as a source of complement components had no demonstrable effect on PMN release either alone or in conjuction with antiserum in these experiments. These data may be relevant to the mechanisms and consequences of the interaction of PMNs and plaque bacteria in the pathogenesis of periodontal disease.  (+info)

Up-regulation of glomerular extracellular matrix and transforming growth factor-beta expression in RF/J mice. (2/3896)

BACKGROUND: RF/J mice were first reported as a murine model of spontaneous glomerulosclerosis by Gude and Lupton in 1960, but the precise histologic characteristics and immunopathological background of this mouse have not been investigated further. METHODS: Measurements of serum levels of immunoglobulins, anti-single strand DNA (anti-ss-DNA) antibody, complement (C3), and circulating immune complex (IC) were performed. Analyses of glomerular histological and immunopathological lesions in association with the detection of mRNA expression of collagen IV, TGF-beta, matrix protein turnover related enzymes, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2) and platelet-derived growth factor (PDGF) were also performed in young (10-week-old) and elderly (60-week-old) RF/J mice with age-matched BALB/C mice as the controls. RESULTS: High levels of serum IgA and IgG from as early as 20 weeks of age were noted in the RF/J mice. Serum anti-ss-DNA antibody of aged RF/J mice increased up to 23% of that of aged MRL-lpr/lpr mice, and serum C3 concentration significantly decreased with age, reaching lower levels than that of BALB/c mice. IgA-IC levels were significantly high compared to BALB/C mice both in the early and late stages of life, whereas IgG-IC levels were high only in mice younger than 20 weeks. Semiquantitative and quantitative analyzes of renal histopathological findings revealed significantly marked and age-related mesangial matrix expansion in RF/J mice, with increasing frequency of global glomerular sclerosis and tubulointerstitial damage. On the other hand, although precise measurements of glomerular cell numbers also showed an apparent augmentation in both young and old RF/J mice compared to BALB/C mice, glomerular cellularity decreased with age in RF/J mice. Immunohistochemical study revealed massive immunoglobulin deposition from a young age in association with significantly higher accumulation of matrix proteins, such as types I and IV collagen and laminin from the early stage of life. In addition, in these glomeruli, transforming growth factor-beta1 (TGF-beta1) was highly expressed both in young and old mice. The mRNA expression of MMP-2 was up-regulated only in the early stage of life. Although PDGF mRNA of RF/J mice was significantly up-regulated in the early stage of life, the differences between the mice disappeared in the late stage of life. CONCLUSIONS: These findings suggest that in RF/J mice, an immunopathological background inducing high serum immunoglobulin and IC levels from the early stage of life is closely related to mesangioproliferative glomerular lesions mediated by PDGF, and that development of massive extracellular matrix accumulation in glomeruli was induced by up-regulated expression of TGF-beta with inappropriate regulation of protein turnover-related enzyme production.  (+info)

Assessment of complement deficiency in patients with meningococcal disease in The Netherlands. (3/3896)

The frequency of complement deficiency in 176 of 7,732 patients with meningococcal disease in the Netherlands from 1959 through 1992 was assessed. Complement deficiency was found in six patients (3%): 3 (7%) of the patients with Neisseria meningitidis serogroup C disease, 1 (2%) of the patients with N. meningitidis serogroup A disease, and 2 (33%) of the patients with infections due to uncommon serogroups and nongroupable strains of N. meningitidis. Of 91 additional patients with meningococcal infections due to uncommon serogroups, 33% also had complement deficiency. Thirty-four of the 36 complement-deficient patients with meningococcal disease who were from 33 families were 5 years of age or older. Twenty-six additional complement-deficient relatives were found. Screening individuals with meningococcal disease due to uncommon serogroups who were 5 years of age or older identified 30 of the 33 complement-deficient families. Only 27% of the complement-deficient relatives had had meningococcal disease. This risk was lower for relatives with properdin deficiency (18%) than for those deficient in the late component of complement (38%). Therefore, pedigree studies are warranted for identifying those complement-deficient persons who require vaccination for meningococcal disease.  (+info)

2-Deoxyglucose selectively inhibits Fc and complement receptor-mediated phagocytosis in mouse peritoneal macrophages II. Dissociation of the inhibitory effects of 2-deoxyglucose on phagocytosis and ATP generation. (4/3896)

Macrophages incubated in 2-deoxy-D-glucose (2-dG)-containing medium showed a marked decrease in cellular ATP content, and were unable to ingest IgG- and complement-coated erythrocytes via the corresponding membrane receptors for these ligands. However, the inhibitory effects of 2-dG on Fc- and C3 receptor-mediated phagocytosis were not a consequence of lowered macrophage ATP levels since addition of glucose or mannose to the culture medium restored the capacity of the macrophages to ingest IgG- and C3-coated particles without increasing ATP levels. These results indicate that Fc- and C3 receptor-mediated phagocytosis (opsonin dependent) differs qualitatively from the ingestion of latex and zymosan particles (opsonin independent); they suggest that the same regulatory molecules govern the responses of phagocytic cells to signals initiated by both the Fc and C3 receptors. The possibility that these molecules are regulated by glycosylation is discussed.  (+info)

The induction of macrophage spreading: role of coagulation factors and the complement system. (5/3896)

Unstimulated mouse peritoneal macrophages, attached to either glass or plastic substrates, responded to factors generated in serum and plasma by spreading and increasing their apparent surface area up to eightfold. Two distinct and dissociable systems were involved. The first appears related to the distinct and dissociable systems were involved. The first appears related to the contact phase of blood coagulation. It is activated by glass and not plastic surfaces, depleted by kaolin adsorption, and inhibited by soybean trypsin inhibitor. In contrast, a separate complement-dependent system can be generated in kaolin-adsorbed plasma. Activation of the complement system can occur either by the alternate or classical pathways and generates a relatively small effector molecule which is dialyzable. These factors presumably influencing the surface membrane and underlying structures may explain the rapid spreading of activated macrophages observed after both infections and chemical peritoneal inflammatory agents.  (+info)

Unexpected crucial role of residue 225 in serine proteases. (6/3896)

Residue 225 in serine proteases of the chymotrypsin family is Pro or Tyr in more than 95% of nearly 300 available sequences. Proteases with Y225 (like some blood coagulation and complement factors) are almost exclusively found in vertebrates, whereas proteases with P225 (like degradative enzymes) are present from bacteria to human. Saturation mutagenesis of Y225 in thrombin shows that residue 225 affects ligand recognition up to 60,000-fold. With the exception of Tyr and Phe, all residues are associated with comparable or greatly reduced catalytic activity relative to Pro. The crystal structures of three mutants that differ widely in catalytic activity (Y225F, Y225P, and Y225I) show that although residue 225 makes no contact with substrate, it drastically influences the shape of the water channel around the primary specificity site. The activity profiles obtained for thrombin also suggest that the conversion of Pro to Tyr or Phe documented in the vertebrates occurred through Ser and was driven by a significant gain (up to 50-fold) in catalytic activity. In fact, Ser and Phe are documented in 4% of serine proteases, which together with Pro and Tyr account for almost the entire distribution of residues at position 225. The unexpected crucial role of residue 225 in serine proteases explains the evolutionary selection of residues at this position and shows that the structural determinants of protease activity and specificity are more complex than currently believed. These findings have broad implications in the rational design of enzymes with enhanced catalytic properties.  (+info)

Phagocytosis of Vibrio cholerae O139 Bengal by human polymorphonuclear leukocytes. (7/3896)

Capsulated bacteria exhibit serum (complement) resistance and resistance to phagocytosis, which result in disseminated infections. Vibrio cholerae O139 strains possess a thin capsule and have been found to be partially serum resistant in a previous study. In the present study, compared to a standard capsulated Klebsiella pneumoniae strain, which showed total resistance to killing by phagocytosis, V. cholerae O139 strains were shown to be only partially resistant, with most strains showing <40% survival. These findings may explain the relative rarity of V. cholerae O139 bacteremia in cholera caused by this organism.  (+info)

Intestinal reperfusion injury is mediated by IgM and complement. (8/3896)

Intestinal ischemia-reperfusion injury is dependent on complement. This study examines the role of the alternative and classic pathways of complement and IgM in a murine model of intestinal ischemia-reperfusion. Wild-type animals, mice deficient in complement factor 4 (C4), C3, or Ig, or wild-type mice treated with soluble complement receptor 1 were subjected to 40 min of jejunal ischemia and 3 h of reperfusion. Compared with wild types, knockout and treated mice had significantly reduced intestinal injury, indicated by lowered permeability to radiolabeled albumin. When animals deficient in Ig were reconstituted with IgM, the degree of injury was restored to wild-type levels. Immunohistological staining of intestine for C3 and IgM showed colocalization in the mucosa of wild-type controls and minimal staining for both in the intestine of Ig-deficient and C4-deficient mice. We conclude that intestinal ischemia-reperfusion injury is dependent on the classic complement pathway and IgM.  (+info)

*Paraproteinemia

The β band consists of transferrin, low-density lipoproteins, and complement system proteins. The γ band is where the ... These are characterized by the presence of any abnormal protein that is involved in the immune system, which are most often ... in the serum protein electrophoresis because there will be an excess of production of one protein. There are two large classes ... In this case, the paraprotein goes under the name of "M-protein" ("M" for monoclonal). If immunoglobulins tend to precipitate ...

*Factor D

... is involved in the alternative complement pathway of the complement system where it cleaves factor B. The protein ... A complement system protein at 2.0 A resolution". Journal of Molecular Biology. 235 (2): 695-708. doi:10.1006/jmbi.1994.1021. ... Finally, the encoded protein has a high level of expression in fat, suggesting a role for adipose tissue in immune system ... The encoded protein is a component of the alternative complement pathway best known for its role in humoral suppression of ...

*Complement deficiency

... is an immunodeficiency of absent or suboptimal functioning of one of the complement system proteins. ... Plasma levels/regulatory proteins (lab study) Disorders of the proteins that act to inhibit the complement system (such as C1- ... causing conditions such as hereditary angioedema Disorders of the proteins that act to activate the complement system (such as ... This rare condition mutates or prevents C3 protein from forming, lowering the immune system's ability to protect. C4: C4 ...

*Regulator of cell cycle RGCC

The protein also translocates to the nucleus in response to treatment with complement system proteins, and can associate with ... or by sublytic levels of complement system proteins that result in activation of the cell cycle. The encoded protein localizes ... Regulator of cell cycle RGCC (RGCC) also known as response gene to complement 32 protein (RGC-32) is a protein that in humans ... "Entrez Gene: RGC32 response gene to complement 32". Fosbrink M, Niculescu F, Rus H (2005). "The role of c5b-9 terminal ...

*Macular degeneration

... on chromosome 6 at 6p21.3 Polymorphisms in genes for complement system proteins: The genes for the complement system proteins ... which is a central protein of the complement system, is strongly associated with the occurrence of AMD. The authors of both ... 2010). "An imbalance of human complement regulatory proteins CFHR1, CFHR3 and factor H influences risk for age-related macular ... Despriet DD, Klaver CC, Witteman JC, Bergen AA, Kardys I, de Maat MP (2006). "Complement factor H polymorphism, complement ...

*Factor I

... may refer to: Complement factor I, a protein of the complement system. Fibrinogen, a protein involved in blood ...

*C8 complex

Complement component 8 is a protein involved in the complement system. It is part of the membrane attack complex (MAC). A ... Figure created in Pymol Complement C8 at the US National Library of Medicine Medical Subject Headings (MeSH) The crystal ...

*Complement component 6

... is a protein involved in the complement system. It is part of the membrane attack complex which can ... Complement component 6 is a protein that in humans is encoded by the C6 gene. ... Müller-Eberhard HJ (1988). "Molecular organization and function of the complement system". Annu. Rev. Biochem. 57: 321-47. doi: ... 2007). "Systematic identification of SH3 domain-mediated human protein-protein interactions by peptide array target screening ...

*Complement system

Over 30 proteins and protein fragments make up the complement system, including serum proteins, and cell membrane receptors. ... The complement system is regulated by complement control proteins, which are present at a higher concentration in the blood ... The complement system is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ...

*Cutaneous small-vessel vasculitis

C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then ... The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. ... immune complexes deposit in vessel walls leading to activation of the complement system. ... Additional symptoms depend on the cause of the vasculitis and if other organ systems are involved. For example, if the ...

*Complement component 7

... is a protein involved in the complement system of the innate immune system. C7 is part of the membrane ... Terminal complement pathway deficiency Complement C7 at the US National Library of Medicine Medical Subject Headings (MeSH). ... This junction alters the configuration of the protein molecules, exposing a hydrophobic site on C7 that allows the C7 to insert ...

*MASP1 (protein)

... protein associated with pattern recognition molecules of the complement system and regulating the lectin pathway of complement ... This protein is not directly involved in complement activation but may play a role as an amplifier of complement activation by ... MASP-1 is involved in the lectin pathway of the complement system and is responsible for cleaving C4 and C2 to form C4b2b, a C3 ... characterization of a novel serine protease involved in activation of the complement system by mannose-binding protein". ...

*C4b-binding protein

... (C4BP) is a protein involved in the complement system where it acts as inhibitor. C4BP has an octopus-like ... Outer membrane protein A from E. coli, Ubiquitous surface protein 1 and 2 from Moraxella. Complement C4b-Binding Protein at the ... proline arginine-rich end leucine-rich repeat protein (PRELP), streptococcal M-proteins, gonococcal porins, ... and necrotic cells is mediated by the Gla domain of protein S and does not affect the ability of C4BP to inhibit complement. A ...

*Overwhelming post-splenectomy infection

So humoral immunity in forms of IgG and complement proteins is the human immune system's response against bacterial capsules. ... In particular, these macrophages are activated when bacteria are bound by IgG antibodies (IgG1 or IgG3) or the complement ... These types of antibodies and complement are immune substances called opsonizers, molecules that bind to the surface of ... The spleen contains many macrophages (part of the reticuloendothelial system), which are immune cells that phagocytose (eat) ...

*C1 complex

The C1 complex (complement component 1, C1) is a protein complex involved in the complement system. It is the first component ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ... The antibodies IgM or certain subclasses of IgG complexed with antigens are able to initiate the complement system: a single ... C1q can also be activated in other ways, for example by binding to pentraxins such as C-reactive protein or directly to the ...

*Complement receptor

... part of the innate immune system. Complement receptors bind proteins of the complement system, and can thus detect pathogens ... Immune system Humoral immunity Janeway, CA Jr; Travers P; Walport M; et al. (2001). "The complement system and innate immunity ... A complement receptor is a receptor of the complement system, ... All four complement receptors bind to fragments of complement ... Peter Parham, The Immune System (2nd ed.), Taylor&Francis "Complement Receptor Deficiency: eMedicine Dermatology". Retrieved ...

*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 ... Lint TF, Zeitz HJ, Gewurz H (November 1980). "Inherited deficiency of the ninth component of complement in man". J. Immunol. ...

*Cancer immunotherapy

The complement system includes blood proteins that can cause cell death after an antibody binds to the cell surface (the ... Antibodies are proteins produced by the immune system that bind to a target antigen on the cell surface. The immune system ... Anti-CD47 antibodies, which block the protein CD47 from telling the cancer host's immune system not to attack it, have been ... Interleukin-2 and interferon-α are cytokines, proteins that regulate and coordinate the behaviour of the immune system. They ...

*Henoch-Schönlein purpura

... a protein of the complement system) in the blood vessel wall. However, overall serum complement levels are normal. On the basis ... Protein loss and high blood pressure, as well as the features on biopsy of the kidney if performed, may predict progression to ... Problems in other organs, such as the central nervous system (brain and spinal cord) and lungs may occur, but is much less ... With kidney involvement, there may be a loss of small amounts of blood and protein in the urine (hematuria and proteinuria), ...

*Complement fixation test

The complement system is a system of serum proteins that react with antigen-antibody complexes. If this reaction occurs on a ... complement proteins in the patient's serum must be destroyed and replaced by a known amount of standardized complement proteins ... A known amount of standard complement proteins are added to the serum. (These proteins are frequently obtained from guinea pig ... The complement proteins will react with these complexes and be depleted. Thus when the sRBC-antibody complexes are added in ...

*Fragment crystallizable region

... region of an antibody that interacts with cell surface receptors called Fc receptors and some proteins of the complement system ... Fc binds to various cell receptors and complement proteins. In this way, it mediates different physiological effects of ... Protein Eng Des. 23 (4): 289-297. doi:10.1093/protein/gzq005. PMID 20150180. "Archived copy". Archived from the original on ... Fab region Protein tag Janeway, CA, Jr.; et al. (2001). Immunobiology (5th ed.). Garland Publishing. ISBN 0-8153-3642-X. ...

*Immunoglobulin G

IgG activates the classical pathway of the complement system, a cascade of immune protein production that results in pathogen ... The relative ability of different IgG subclasses to fix complement may explain why some anti-donor antibody responses do harm a ... Nevertheless, it remains true that both human and mouse antibodies have different abilities to fix complement and to bind to Fc ... Given the opposing properties of the IgG subclasses (fixing and failing to fix complement; binding and failing to bind FcR), ...

*Complement component 1s

... activated complement C1s, complement C overbar 1r, C1s) is a protein involved in the complement system. C1s is part of the C1 ... Müller-Eberhard HJ (1988). "Molecular organization and function of the complement system". Annual Review of Biochemistry. 57: ... "The human complement system serine proteases C1r and C1s and their proenzymes". Methods in Enzymology. 80 Pt C: 26-42. doi: ... "Entrez Gene: C1S Complement component 1, s subcomponent". Luo C, Thielens NM, Gagnon J, Gal P, Sarvari M, Tseng Y, Tosi M, ...

*C3a receptor

... is a G protein-coupled receptor protein involved in the complement system. The receptor binds to complement component C3a, ... Sim RB, Laich A (October 2000). "Serine proteases of the complement system". Biochemical Society Transactions. 28 (5): 545-50. ... C3AR1 protein, human at the US National Library of Medicine Medical Subject Headings (MeSH) Human C3AR1 genome location and ... Roglic A, Prossnitz ER, Cavanagh SL, Pan Z, Zou A, Ye RD (February 1996). "cDNA cloning of a novel G protein-coupled receptor ...

*Cholesterol embolism

... complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in ... Both the central nervous system (brain and spinal cord) and the peripheral nervous system may be involved. Emboli to the brain ... Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic ... If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; ...

*Shotgun proteomics

Cells containing the protein complement desired are grown. Proteins are then extracted from the mixture and digested with a ... This analysis allows researchers to profile various biological systems. Peptides that are degenerate (shared by two or more ... including low-abundance proteins like transcription factors and protein kinases. They were also able to identify 131 proteins ... aberrant proteins, and membrane proteins. Shotgun proteomics emerged as a method that could resolve even these proteins. ...
highlighting the link between complement gene expression and IQ, in both schizophrenic patients and healthy controls. The study demonstrated a broad association between variations in complement gene expression and perturbed neurodevelopment. We were particularly interested to see that the final sentence of the paper stated that When complement gene-sets are taken as a whole, their relevance is to neurodevelopment, not illness . Their conclusion rightly touches on the emerging understanding of non-immune roles for complement in diverse biological processes (Hawksworth et al., 2018) .The complement group of proteins is ancient in evolutionary terms. Recognised complement components are found strewn throughout the animal kingdom including in rudimentary diploblastic species (Kimura et al., 2009) . In the human adult, complement functions as an essential pillar of the innate immune system. It is activated by various noxious stimuli and results in the production of the anaphylatoxins and membrane attack
We have been interested in developing a complement dependent opsonophagocytic assay for Neisseria meningitidis serogroups A and C. Our problem is that when we add a complement source (baby rabbit) we get (as expected) bactericidal killing. We have tried to remove one of the terminal complement components but without much success (can remove component(s) but the removal process reduces the lytic complement activity when we reconstitute with the purified complement component). We have had success using a serum from a C7 defficient patient, however, this complement source is in limited supply. QUESTIONS: 1. is anyone else working on this? have you had success? 2. is there a method to remove terminal components in human sera that does not reduce complement activity when the component is added back? can this method be used for large vols. (600 ml)? 3. did I miss something in the literature? 4. any ideas or suggestions? P#: (404)639-3622 F#: (404)639-3115 George ...
Complement is the term used to describe a group of serum proteins that are critically important in our defense against infection. There are deficiencies of each of the individual components of complement. Patients with complement deficiencies encounter clinical problems that depend on the role of the specific complement protein in normal function.
Porcine complement regulators protect aortic smooth muscle cells poorly against human complement-induced lysis and proliferation: consequences for xenotransplantation. Xenotransplantation 12 (3) , pp. 217-226. 10.1111/j.1399-3089.2005.00217.x ...
Looking for Complement system? Find out information about Complement system. The sequential activation of complement proteins resulting in lysis of a target cell Explanation of Complement system
Teacher Certification Training. Competency 046: Structure and Function of Living Things. Characteristics of organisms from major taxonomic groups; How structure complements function in cells; How structure complements function in tissues, organs, organ systems and organisms; Human body systems and their functions; How organisms obtain and use energy and matter; Structure and function of basic chemical components of living things.
... The activated complement system recognizes and eliminates invading microorganisms and thus is beneficial for the host.
Detailed description of complement system including classical pathway, alternate pathway and lectin pathway. Components of complement system includingC1, C2, C3, C4, C5, C6, C7, C8, C9, C1-INH, C3a-INA, Factors H and I, C3a-INA, C4-BP and Factor I, C3a-INA, Protein S (vitronectin).
The reduction in C in this study was accomplished, as in our previous study (44), by use of CVF, which activates the alternative pathway of the C cascade (10). It forms a complex with factor B, CVF Bb, which is functionally analogous to C3b Bb, the natural C3 convertase that cleaves catalytically the α-chain of C3. The difference between the two compounds is that CVF Bb is highly resistant to the normal control mechanisms that limit the activity of C3b Bb, so that fluid-phase C activation continues unabated, drastically depleting C. Consequently, absent the substrates from which they are produced, all the subsequent C components are also depleted; hence, hypocomplementemia results. Since the present data showed, in confirmation of our earlier observations (44), that CVF-induced hypocomplementemia, as indicated by a decreased serum CH100 activity, impaired the febrile response of conscious guinea pigs to systemic LPS, some or all of the fragments from C3 to C9 must be important for fever ...
The use of monoclonal antibodies as immunotherapeutic agents for specific cancers is now an accepted clinical practice, although the mechanisms behind their beneficial effects are not fully understood. One mechanism involves complement-mediated cytotoxicity, whereby the monoclonal antibody induces complement deposition on the targeted cancer cells, leading to the stimulation of complement receptor 3 (CR3)-dependent leukocyte killing of the tumour cells. Triggering of this cytotoxicity, however, requires a second stimulus, such as that mediated by β-glucan carbohydrates, leading to proposals that these carbohydrates could be used as adjuvants for these treatments. β-Glucans can also directly potentiate host protective responses against cancer and there have been a number of clinical trials using these carbohydrates with promising results. Our project is laying the foundation for a better understanding of the molecular mechanisms by which β-glucans exert their anti-cancer effects, which will ...
Application Index: Complement Proteins offered by Sigma-alderich online.The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. This cascade ultimately results in induction of the inflammatory response, phagocyte chemotaxis and opsonization, and cell lysis.
The complement system is a key component of the innate immune system that is involved in eliminating unwanted self and nonself material via cellular and humoral mechanisms
The Complement System is one of the subject in which we provide homework and assignment help. Our feature includes 24x7 live online statistics tutors available to help you. You can get speedy and cost Immunology help at assignmenthelp.net
Use Affi-Gel Blue Gel for rapid albumin removal, enzyme purification, and the separation and purification of plasma proteins inlcuding human serum complement.
Bio-Rad Antibodies (formerly AbD Serotec) is the research antibody division of Bio-Rad, the worlds leading life science company.
Study Flashcards On Immuno Five: Complement at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
For performing VDRL of serum , we heat serum to inactivate complement proteins which may otherwise interfere , but why dont we do same for CSF even though it too has complement proteins in it?. Is it because of lesser stability of WBCs in CSF( which is hypotonic) and on heating may rupture to release cardiolipin? But I cant comprehend how its worse than having complement proteins?. ...
Introduction to the Complement System The innate and adaptive immune systems are no longer considered as distinct separate entities but are now recognized
this suit was fun to wear and i got a lot of complements on the fringe beads. the beads didnt get annoying in the water either! throw on some shorts and it becomes a cute top ...
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There is wide variation of infections associated with complement deficiency depending on which complement protein and activation pathway is affected(Skattum et al 2011). Some complement deficiencies caries risk of infection, other mainly associated with autoimmune diseases. Some genetic and molecular defects has been identified to be associated complement deficiencies. The deficiencies in alternative pathway and terminal pathway is commonly presented with markedly increased susceptibility to Neisserial infections. Properdin deficiency (PD) has been reported in cases of severe meningococcal infections (Fijen et al 1999), recurrent otitis media and pneumonia (Schejbel et al 2009). PD has been identified as X-linked inheritance. Around 500 published cases of PD with Neisserial infections world wide. Neisserial meningitidis meningitis and Streptococcal Pneumonie also has been reported in complete Factor D deficiency. The TP components deficiencies has been reported association with Neisserial ...
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The normal range for a complement C4 blood test is 16 to 48 milligrams per deciliter (mg/dL), or 0.16 to 0.48 grams per liter (g/L). Your complement levels will often shoot up dramatically just after an infection or injury. When your complement system is activated in response to ongoing disease such as lupus, levels usually go down. You can inherit a deficiency in your complement C4, but it is much more common to acquire a deficiency. If only your C4 complement level is low, and all other complement components are normal, it is usually because of an inherited component deficiency. More often, you will have lowered levels of several complement components at once. This is the result of an acquired disease. If your C3 and C4 levels are reduced, this may be a sign that ...
19 Autoimmunity and Inherited Complement Deficiencies How does SLE form with complement deficiencies? How does SLE form with complement deficiencies? -Failure to clear autoantigens (apoptotic cells) -Immature dendritic cells uptake the antigen in the presence of inflammatory cytokines causing them to mature into antigen presenting dendritic cells - Presents to T-Cell -Autoreactive B-Cells take up antigen from apoptotic cells and (with the help CD4+ Th2-Cells) transform into plasma cells that secrete autoantibody QUIZ TIME Q: Dendritic Cells present antigen with MHC Class I or MHC Class II? A: MHC Class II - It is an APC (antigen presenting cell) Q: MHC Class II molecules present antigen derived from intracellular or extracellular processes? A: Extra-cellular (e.g. apoptotic cells) Q: MHC Class II molecules stimulate CD4 or CD8 cells A: CD4 (IIx4=8, Ix8=8) Q: In this scenario with the APC being a dendritic cell - the CD4 T-lymphocyte it interacts with is a Th1 or Th2? A: Th1 is chiefly involved ...
Radioimmune assays were developed to assay the binding of complement components C1q, C1s and C4 to antibody aggregates and to cell-bound antibody. The binding of the components was compared with the haemolytic activity and with the capacity to form the C3 convertase activity in the presence of excess C2. The destruction of whole complement and of C4 activity is similar per 1,000 molecules of antibody in aggregates and cell-bound antibody, as is the binding of C1g and C1s, the latter being in a 1:2 molar ratio. The binding of C4 is about 12 times greater, per 1,000 molecules of antibody, on cells than in aggregates. However, the effective C4 molecules, as judged by the formation of C3 convertase activity, are much more similar on cells and aggregates. An assembly mechanism of the early components of complement on antibody-coated cells, which is compatible with these results, is suggested. ...
The complement system provides a fundamental component of the body's immune response to invading microorganisms. This chapter highlights the various roles of the complement system in the orchestration of the immune response towards microbial infections, gives examples of microbial strategies to evade complement-mediated clearance, and discusses how acquired and inherited complement deficiencies may predispose an organism to infectious disease. Complement is activated by three pathways: the classical pathway, the alternative pathway, and the lectin pathway. The lectin pathway is activated by carbohydrate recognition molecules that bind to polysaccharide on the surface of a pathogen. Factor B, factor D, and properdin (factor P) are specific components of the alternative pathway of complement activation. The complement activation is tightly regulated by membrane-bound and fluid-phase regulatory components to avoid runaway activation of the enzymatic cascade that could lead to excess host tissue damage
The role of complement activation products in sepsis and in complications such as MOF is a debatable issue. There is fairly good evidence to suggest that, in the absence of complement such as in complement-depleted animals (14) or in C3 or C4 mutant mice lacking this critical complement component (18, 19), animals are highly susceptible to the early and lethal effects of experimental sepsis. These observations reinforce the long-standing concept that the complement system functions as a critical protective pathway via products such as C3b and iC3b. Evidence also exists that, during sepsis, extensive activation of the complement system occurs resulting in loss of homeostasis, which may in some manner compromise survival. Intravenous infusion of C5a into dogs generated a shock syndrome characterized by portal blood pooling and an associated decrease in venous return, cardiac output, and arterial pressure (20). In experimental sepsis caused by massive i.v. infusion of live, Gram-negative bacteria ...
When the complement system is activated, it triggers a variety of events leading to cleavage of one component known as C5. Once C5 is cleaved, a variety of events occur that propagate the formation of the membrane attack complex. This member attack complex generates pores, or holes, in cells ultimately leading to the cells demise. So when you have such a powerful system, regulators of the system are needed. These regulators sit on the outer membrane of cells, so the complement system recognizes that these cells are of the self. When those regulators are missing, as is the case in PNH, this leads to the destructions of the cells that are missing these protein shields.. Some of those shields, (2 proteins known as CD 55 and CD 59) are anchored the cell surface by a tail. We call this tail a GPI anchor - but in PNH this GPI anchor is missing because of a mutation in a gene called PIG-A. This defective gene leads to cause the cells inability to form this GPI anchor. So the complement regulator ...
In this study, we showed that blocking complement activation accelerates the early healing rate in a mouse model of cutaneous wound healing. We also found that the components of the complement system responsible for this effect include C3, C5, and signaling through C5aR1, but not C5aR2 or C3aR. Furthermore, reconstitution of C3-deficient animals with purified human C3 or serum from C3+/+ mice abrogated the effect, confirming the involvement of complement in the process. The absence of these molecules resulted in a reduction in the intensity of inflammation involved in the initial events of healing. We postulate that the reduced inflammation allowed the process to advance faster to the subsequent events of healing (proliferation, maturation), thus accelerating the whole process. Moreover, we observed an increase of vascularization accompanied by a significantly higher presence of mast cells in complement-deficient mice.. A major role of complement effectors is to attract, activate, and control ...
Each pathway follows a sequence of reactions to generate a protease called a C3 convertase. The active protease is retained at the pathogen surface, and this ensures that the next complement zymogen in the pathway is also cleaved and activated at the pathogen surface. By contrast, the small peptide fragment is released from the site of the reaction and can act as a soluble mediator.. The early events of all three pathways of complement activation involve a series of cleavage reactions that culminate in the formation of an enzymatic activity called a C3 convertase, more The C3 convertases formed by these early events of complement activation are bound covalently to the pathogen surface. Here they cleave C3 to generate large amounts of C3bthe main effector molecule of the complement system, and C3a, a peptide mediator of inflammation.. The C3b molecules act as opsonins; they bind covalently to the pathogen and thereby target it for destruction by phagocytes equipped with receptors for C3b. These ...
Definition of Cobra venom factor with photos and pictures, translations, sample usage, and additional links for more information.
Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect the unnecessary activation of complement components. Objective: To investigate the expression of CD55 and CD 59 complement regulatory proteins in RA patients. Subjects and Methods: Fifty proved rheumatoid arthritis patients participated in this study and their blood were collected for investigations. CD55 and CD59 molecules expression on the erythrocytes was assayed using primary monoclonal antibody and secondary FITC conjugated Ab, then the prepared samples were run with a FACSCalibur flowcytometer (Becton-Dickinson) and the obtained data was analyzed using a Cell Quest software package. To evaluate the complement function, CH50 was performed using patient sera. All experiments were done with a matched
BSc, 1983, University of Burdwan, India. Research Interests Dr. Hudas research interest is focused on Immunology-Therapy for Autoimmune disease SiRNA mediated silencing of complement gene expression as therapy for experimental autoimmune mouse Myasthenia gravis (EAMG), EAMG in IgG1 deficient mice and therapeutic response of recombinant cobra toxin in EAMG.. Recent Publications. Search PubMed Database for Publications ...
The coding capacity of the genome is not controlled solely by DNA sequences, but is rather fine-tuned through epigenetic factors and the nuclear structure. In the Yildirim lab, we study how epigenetic mechanisms, particularly those that are mediated by long noncoding RNAs (ncRNAs), complement gene expression, impact genome stability and define cell fate decisions. Other research in the lab focuses on understanding how chromatin-nuclear envelope interactions mediate gene expression programs in stem cells. We are interested in defining the molecular bases of these interactions and delineating their significance in driving gene expression and genome functions. We approach these two main areas of research by utilizing a variety of genetic, cell biological and genomics tools using mouse stem cells and mouse models. In the long run, a detailed understanding of the genetic, epigenetic, and cellular mechanisms that are mediated by long ncRNAs and nuclear structure will allow us to explore their causal ...
The classical pathway begins with the formation of antigen-antibody complex (immune complex). When an antigen enters the body, the antibody (IgM/IgG) binds to it. This induces conformational changes in the Fc portion of the antibody which exposes a binding site for C1 protein. Hence, the antibody activates the complement system only when bound to an antigen.. C1 is a large, multimeric, protein complex composed of one molecule of C1q and two molecules each of C1r and C1s subunits. C1q binds to the antigen bound antibody (Fc portion). C1r and C1s are proteases which help to cleave C4 and C2.. The immune complex bound to C1 calls another protein C4 which is cleaved into C4a and C4b. C4a goes away whereas activated C4b attaches to the target surface near C1q. Now, C4b attracts C2 which is also cleaved into C2a and C2b. C2a binds C4b forming the C4b2a complex whereas C2b goes away. The active C4bC2a activates C3. The C4b2a complex is also known as C3 convertase as this converts C3 into an active form ...
A new cluster of complement component genes, including C4BP, C3bR, and FH, is described. Family segregation data indicate that FH is linked to the genes for C4-bp and C4bR, previously reported to be linked and to maintain linkage disequilibrium. This cluster is not linked to the major histocompatibility complex, which contains the genes for the complement components, C4, C2, and factor B, or to the C3 locus. These data further suggest that the organization of genes for functionally related proteins in clusters may be a rule for the complement system. ...
An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. This system can be activated in a convertase-independent manner from intracellular stores of the complement component C3. The source of these stores has not been rigorously investigated. In the present study, Western blotting identified a band corresponding to C3 in freshly isolated human peripheral blood cells that was absent in corresponding cell lines. One difference between native cells and cell lines was the time absent from a fluid-phase complement source; therefore, we hypothesized that loading C3 from plasma was a route of establishing intracellular C3 stores. We found that many types of human cells specifically internalized C3(H2O), the hydrolytic product of C3, and not native C3, from the extracellular milieu. Uptake was rapid, saturable, and sensitive to competition with unlabeled C3(H2O), indicating a specific mechanism of loading. Under steady-state conditions, approximately 80% ...
An intracellular complement system (ICS) has recently been described in immune and nonimmune human cells. This system can be activated in a convertase-independent manner from intracellular stores of the complement component C3. The source of these stores has not been rigorously investigated. In the present study, Western blotting identified a band corresponding to C3 in freshly isolated human peripheral blood cells that was absent in corresponding cell lines. One difference between native cells and cell lines was the time absent from a fluid-phase complement source; therefore, we hypothesized that loading C3 from plasma was a route of establishing intracellular C3 stores. We found that many types of human cells specifically internalized C3(H2O), the hydrolytic product of C3, and not native C3, from the extracellular milieu. Uptake was rapid, saturable, and sensitive to competition with unlabeled C3(H2O), indicating a specific mechanism of loading. Under steady-state conditions, approximately 80% ...
This is a collection of nine reviews focusing on the strategies used by bacteria, viruses and parasites to avoid detection or destruction by the hosts immune system. It begins with an overview of the subversion process and its effects on complement, natural killer cells and other parts of the mucosal innate immune system. This is followed by general reviews of the subversive techniques of viruses, bacteria and helminths. Lastly, there are three papers dealing more specifically with the humoral immune response and dendritic cell reaction to viruses, and a description of the measles virus serving as a model for the mechanisms of inhibition of human antiviral defenses ...
Russell, J H.; Masakowski, V; Rucinsky, T; and Phillips, G, "Mechanisms of immune lysis. Iii. Characterization of the nature and kinetics of the cytotoxic t lymphocyte-induced nuclear lesion in the target." (1982). Subject Strain Bibliography 1982. 2733 ...
In the late 19th century, blood serum was found to contain a "factor" or "principle" which was capable of killing bacteria. In 1896, Jules Bordet, a young Belgian scientist in Paris at the Pasteur Institute, demonstrated that this principle could be analyzed into two components: a heat-stable and a heat-labile component. (Heat-labile meaning that it lost its effectiveness if the serum was heated.) The heat-stable component was found to confer immunity against specific microorganisms, while the heat-labile component was found to be responsible for the non-specific antimicrobial activity conferred by all normal serum. This heat-labile component is what we now call "complement". The term "complement" was introduced by Paul Ehrlich in the late 1890s, as part of his larger theory of the immune system. According to this theory, the immune system consists of cells which have specific receptors on their surface to recognize antigens. Upon immunization with an antigen, more of these receptors are formed, ...
The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
We offer specialty testing for infectious disease serology, immunocompetencies, immunodeficiencies, complement deficiencies, monoclonal and polyclonal gammopathies, and immunoglobulin deficiencies. ARUP is one of few labs in the country offering specific panels for autoimmune disorders (e.g., myositis and neurologic syndromes) based on clinically relevant biomarkers.. ...
Health update on me: All my blood work came back excellent and my doctor was very impressed. The only things to slightly worry about was my C3 blood test, my ANA blood test and protein urine test. The Complement C3 blood test, according to the national library of medicine, is a blood test that measures the activity of a certain protein that is part of the complement system. The complement system is a group of proteins that move freely through your bloodstream. The proteins work with your immune system and play a role in the development of inflammation. My C3 was low which is common with SLE lupus patients. My ANA score came back elevated, which just means that my lupus is very so slightly active and I still had protein in my urine (but only 30mg!). All in all, nothing to worry about ...
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January 4, 2013: Dr. Bob Zavala (U.S. Naval Observatory, Flagstaff) has requested AAVSO assistance in obtaining multicolor photometry of the bright triple system b Per in order to prepare for and detect a possible eclipse of the AB components by the C component predicted for 2013 January 23. At 4.5V, b Per, which is also a radio source, is an excellent target for photoelectric photometrists and DSLR observers. ...
January 4, 2013: Dr. Bob Zavala (U.S. Naval Observatory, Flagstaff) has requested AAVSO assistance in obtaining multicolor photometry of the bright triple system b Per in order to prepare for and detect a possible eclipse of the AB components by the C component predicted for 2013 January 23. At 4.5V, b Per, which is also a radio source, is an excellent target for photoelectric photometrists and DSLR observers. ...
Hydrate your body after a long nights rest, it eliminate toxins as well as reduce uric acid from your joints. The vitamin C component acts to defy aging...
Sberro-Soussan, B. Severino, N.S. Sheerin, A. Trivelli, L.B. Zimmerhackl, T. Goodship, and C.1,2 This syndrome is due to defects in regulation of the complement system. These defects are inherited, acquired, or both, plus they bring about chronic, uncontrolled activation of the complement system1-4 which leads to platelet, leukocyte, and endothelial-cell activation and systemic thrombotic microangiopathy.1,5-9 […]. Read More ...
Hereditary Factors:, Life-History Effects:, Serology: Antigen, Genes: Hc - Hemolytic complement, MuBl,, Strains: A/HE, AKR, BALB/C, BSVS, CBA, CE, C57BL, C57BL/6, C57BR/CD, C57L, C58, DBA/1 (12), DBA/2 (212), MA (MARSH), MO, P, SIMPSON, PL (PLA, PLB), RF (W), SJL, SL, SM, SWR, T6T6, WHT (WH/HT), 129, BUB. ...
Definition: Total complement of genes contained in a cell or virus; commonly used to refer to all genes present in one complete haploid set of chromosomes in eukaryotes. Source: Essential Genetics: A genomics perspective (2006) 4th Ed. ...
The RIQAS Specific Protein EQA programme is designed to monitor the performance of up to 26 serum proteins including CRP, ASO, RF, Complement Proteins and Immunoglobulins. Three flexible size options are available to help reduce waste and costs.. Available Applications. http://inserts.randox.com/out.php. Parameters ...
Purpose: Complement activation and oxidative stress have been increasingly implicated in the pathogenesis of AMD. Complement activation products have been detected in Bruchs membrane and drusen from patients, indicating that in AMD, complement attack likely occurs primarily on the RPE basal surface. Herein, we describe a model used to investigate the effect of oxidative stress on complement-mediated RPE cell injury, whereby complement attack was initiated with an RPE-specific priming antibody on the basal surface of differentiated human RPE cells.. Methods: ARPE-19 cells and RPE cells from 2 donors were cultured for one month on collagen-coated porous supports in DMEM-F12 containing 1% FBS. Transepithelial resistance (TER) was recorded, apical microvilli and tight junctions were identified by transmission electron microscope, and ZO-1 was examined by immuno-fluorescent staining. Cytokeratin-18 staining was used to confirm the epithelial nature of RPE cells. The cells were basally exposed for 2 ...
Being a major first line of immune defense, the complement system keeps a constant vigil against viruses. Its ability to recognize a large panoply of viruses and virus-infected cells, and trigger the effector pathways, results in neutralization of viruses and killing of the infected cells. This selection pressure exerted by complement on viruses has made them evolve a multitude of countermeasures. These include targeting the recognition molecules for avoidance of detection, targeting key enzymes and complexes of the complement pathways like C3 convertases and C5b-9 formation - either by encoding complement regulators or by recruiting membrane-bound and soluble host complement regulators, cleaving complement proteins by encoding protease, and inhibiting the synthesis of complement proteins. Additionally, viruses also exploit the complement system for their own benefit. For example, they use complement receptors as well as membrane regulators for cellular entry as well as their spread. Here, we provide an
TY - JOUR. T1 - Risk of non-Hodgkin lymphoma in association with germline variation in complement genes. AU - Cerhan, James R. AU - Novak, Anne J. AU - Fredericksen, Zachary S.. AU - Wang, Alice H.. AU - Liebow, Mark. AU - Call, Timothy G.. AU - Dogan, Ahmet. AU - Witzig, Thomas Elmer. AU - Ansell, Stephen Maxted. AU - Habermann, Thomas Matthew. AU - Kay, Neil Elliot. AU - Slager, Susan L. PY - 2009/6. Y1 - 2009/6. N2 - Germline mutations in complement genes have been associated with susceptibility to infections and autoimmune diseases, conditions that are associated with non-Hodgkin lymphoma (NHL) risk. To test the hypothesis that common genetic variation in complement genes affect risk of NHL, we genotyped 167 single nucleotide polymorphisms (SNPs) from 31 genes in 441 NHL cases and 475 controls. Principal components (PC) and haplotype analyses were used for gene-level tests of NHL risk, while individual SNPs were modelled as having a log-additive effect. In gene level PC analyses, C2 (P = ...
We previously described a simplified quantitative hemolytic assay for classical pathway (CP) hemolytic function in serum that has been shown to correlate with the 50% hemolytic complement (CH50) assay. In the present study, we used this assay to compare CP functions; plasma levels of C3, C4, and C3dg; and ratios of C3dg to C3 in healthy individuals and patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) with different degrees of complement activation. A significant depression in CP function and levels of C4 and C3 and increased C3dg levels and C3dg/C3 ratios were observed in the SLE patients. In patients with RA, CP function was normal, whereas C3, C4, and C3dg levels and the C3dg/C3 ratio were elevated. The SLE results are compatible with systemic complement consumption, whereas the RA data suggest an acute-phase reaction with a normal C3 catabolic rate. To facilitate the handling of patient samples, we also developed a method to restore the hemolytic function of ...
Abstract Background: An optimal dosage and infusion regime for protamine reversal of heparin after cardiopulmonary bypass is important. Methods: Protamine dosages of either 2mg/kg or 4mg/kg
CRP seems to be not only a biomarker for atherosclerosis but also a mediator of plaque formation.3 By binding to enzymatically degraded low-density lipoprotein, CRP is able to activate the classical pathway of complement,13 serving as a potential link between complement activation and atherosclerosis.9,10 To protect against complement-mediated cell lysis, nucleated cells express complement inhibitor proteins on their surface. By upregulating the expression of these proteins in endothelial cells, CRP may serve to protect ECs from complement-mediated injury.. The ability of CRP to bind to nucleated cells and cause complement activation without cytolysis14 has been largely attributed to its ability to recruit the inhibitory plasma protein factor H.15 However, our results indicate that CRP may play a more active, protective role by stimulating the expression of DAF, CD46, and CD59 in endothelial cells. The kinetics of DAF expression were analyzed in greater detail because DAF seems to be the most ...
Background Glaucoma is an age-related neurodegenerative disorder involving the loss of retinal ganglion cells (RGCs), which results in blindness. Studies in animal models have shown that activation of inflammatory processes occurs early in the disease. In particular, the complement cascade is activated very early in DBA/2J mice, a widely used mouse model of glaucoma. A comprehensive analysis of the role of the complement cascade in DBA/2J glaucoma has not been possible because DBA/2J mice are naturally deficient in complement component 5 (C5, also known as hemolytic complement, Hc), a key mediator of the downstream processes of the complement cascade, including the formation of the membrane attack complex. Methods To assess the role of C5 in DBA/2J glaucoma, we backcrossed a functional C5 gene from strain C57BL/6J to strain DBA/2J for at least 10 generations. The prevalence and severity of glaucoma was evaluated using ocular examinations, IOP measurements, and assessments of optic nerve damage and RGC
The serine-proteinase domain is responsible for the proteolytic events that occur during complement activation. The sequences of nine serine proteinases of known crystal structure were compared with the serine-proteinase sequences in the six complement proteins C1r, C1s, C2, factor B, factor I and factor D to assess the degree of structural homology of the latter with the crystal structures. All sequence insertions and deletions were readily located at the protein surface. The internal location of disulphide bridges and the surface location of putative glycosylation sites are compatible with this structure. Secondary-structure predictions for the sequences were fully consistent with the crystal structures. It is concluded that the double subdomain beta-sheet motif is retained in the complement sequences, but that localized differences are observed for factor I, C2 and factor B. ...
Both complement and Fc regions of IgA 1 have been shown to enhance the uptake of antigens by antigen presenting cells (Fang, et. aI., 1998, Foged, et. aI., 2005, Perrin-Cocon, et. aI., 2004). However, the utilization of complement and IgA1 antibodies in enhancing the uptake of antigens by dendritic cells has not been examined to date. The aims of this research included attaching complement to antidansyl IgA 1 antibodies followed by induction, activation, and examination of dendritic cells incubated with the antigen-antibody immune complexes to determine potential interactive relationships. Complement was linked to the Fc region of anti-dansyl IgA 1 antibodies using a procedure to activate complement while the IgA 1 was bound to a dansylated Sepharose 4B affinity column. The eluted complement-coated IgA 1 antibodies were mixed with dansylated albumin to form the complement-coated IgA1-immune complexes. Then, the immune complexes were incubated with PBMCderived dendritic cells to induce maturation ...
c-C3BP or rGAPDH was observed (Figure 3c, d). The H.c-C3BP or rGAPDH interaction with C3 was specific and strong, which was evident from the fact that the column-bound C3 was eluted at high salt wash (0·5 m NaCl) or by lowering the pH to 2·2. To test whether H.c-C3BP or rGAPDH binding to C3 would influence complement function, a simple haemolytic assay was performed where the lysis of sensitized sheep erythrocytes by serum complement proteins was measured. As shown in Figure 3(e, f), a dose-dependent inhibition of erythrocyte lysis by H.c-C3BP and rGAPDH was observed. To rule out that the observed inhibition was not due to suppression of the classical pathway, binding of C1q protein by H.c-C3BP was. measured. No interaction among these proteins was evident in the microtitre plate assay (not shown). To confirm check details whether the inhibition of erythrocyte lysis by H.c-C3BP or rGAPDH was due to suppression of C3 activation, the formation of membrane attack complex (MAC) was measured on the ...
What is Complement Component Gene? Definition of Complement Component Gene. Complement Component Gene FAQ. Learn more about Complement Component Gene. Complement Component Gene facts.
Although risk factors for poor prognosis in patients with IgAN have been reported previously [1, 2], it is still difficult to accurately estimate renal prognosis in these patients. Although serum levels of C3 and C4 frequently fluctuate within the normal range in IgAN patients, studies have increasingly focused on the role of complement in the pathogenesis of IgAN [14-17]. However, the relationship between serum complement levels and the renal prognosis of patients with IgAN remains controversial.. There were studies discussing the relationship between serum C3 levels and the prognosis of IgAN. Kim et al. reported that low serum C3 at the time of renal biopsy was an independent risk factor for poor prognosis [18]. Lbels et al. also found that higher serum C3 at the end of follow up were associated with adverse outcomes, but lower baseline serum C3 levels were unrelated to prognosis [19]. Conversely, Komatsu et al. did not identify any difference in serum C3 levels between patients with severe ...
The complement system is a major humoral component of vertebrate defenses for tagging and killing target microorganisms. Recent molecular analyses have uncovered a striking feature of bony fish complement, namely that several complement components are encoded by multiple genes. In this review, the structural diversity of C3, C4, C5, factor B, C2, C1r/s and MASP are discussed with special reference to their functional differentiation, mainly focusing on the common carp (Cyprinus carpio), a tetraploidized teleost. In carp, all the members (C3, C4, C5 and a non-complement protein alpha2-macroglobulin) of the thioester-containing protein family are present in multiple isotypes, differing in the primary structures of various functional sites. Three factor B/C2-like isotypes identified in carp showed distinct expression pattern (sites and inducibility), with one behaving as an acute-phase reactant. Two C1r/C1s/MASP2-like isotypes also contain an amino acid substitution that likely affects their substrate
IC-mediated Complement Activation, Complement Control Proteins, and Fcγ ReceptorsComplement Is Activated by Infected E and by E Breakdown Products; Activation of the AP of Complement Can Opsonize Uninfected E with C3b: Potential Consequences; Paroxysmal Nocturnal Hemoglobinuria (PNH) as a Model for Extravascular Clearance of C3d-Opsonized E; Additional Evidence for Activation of the Alternative Pathway; Acidemia: Another Possible Activator of Complement; Complement Activation by the MBL Pathway; Changes in the Spleen Possibly Mediated by Complement During Malarial Infections: Speculations ...
... is produced by our E.coli expression system and the target gene encoding Asn679-Arg755 is expressed.
Regulation of complement activity by immunoglobulin. I. Effect of immunoglobulin isotype on C4 uptake on antibody-sensitized sheep erythrocytes and solid phase immune complexes.
Previous studies have shown that complement opsonization is required for efficient phagocytosis of dying cells in vitro (6, 7) and that uptake of these opsonized cells is associated with expression of the antiinflammatory cytokine, TGF-β (6). Three observations, namely that C1q binds to apoptotic cells in vitro (10), that apoptotic cells accumulate in the kidneys of mice deficient in C1q (4), and that complement activation on apoptotic cells promotes phagocytosis of these cells by macrophages in vitro, suggest a pivotal role for complement in noninflammatory clearance of dying cells. Here, we report that IgM antibodies in normal individuals are quantitatively most important for C1q binding and C3b/bi activation on the apoptotic cell surface and that these natural antibodies bind to lysophosphorylcholine that is exposed on cells undergoing apoptosis.. Since IgM bound to apoptotic cells by the Fab, rather than the Fc, portion of the Ig, binding could be attributed to antibody recognition of an ...
By the use of chambers containing two compartments with an interposed micropore filter, chemotaxis of polymorphonuclear leukocytes (PMNs) in vitro was studied employing various agents that fixed serum complement (C). Antigen-antibody complexes, zymosan, and aggregated human gamma globulin, in the presence of fresh rabbit, guinea pig, or mouse serum resulted in the migration of PMNs through the micropore filter. Pepsin-degraded rabbit antibody or unaltered duck serum containing antibody did not exhibit such activity after addition of antigen. Heating of the serum before treatment or the presence of EDTA prevented the generation of the chemotactic factor. The chemotactic factor could not be generated in whole serum from rabbits genetically deficient in C. However, the defect in this rabbit serum could be corrected by addition of rabbit or human C6. Serum of B10.D2 mice deficient in hemolytic C also yielded poor chemotactic activity. Interaction of the first four reacting components of guinea ...
Neurology news, research and treatment studies for epilepsy, neurodegenerative disorders, patients with MS and other brain and central nervous system disorders and diseases.
Melted terminal components on Red Brick battery - posted in Batteries/Power: Hi All, I know this isnt really Steadicam related, but I was hoping I could draw on your experience and knowledge with this nasty situation. We hired a RED from one of my freinds to use at the BSC show, and he has just told me that a terminal on the charger and on one battery has melted. I have seen no photos so im not sure exactly what he means, but he is saying hte plastic parts around the power terminal...
Influence of serum complement and rheumatoid factor on detection of immune complexes by the C1q and monoclonal rheumatoid factor solid-phase assay ...
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Both eicosanoid generation and the complement system have long evolutionary histories predating the emergence of the vertebrates over 500myr ago. This study investigated the interplay between these two systems in an example of a bony fish, the rainbo
anti-Complement C4 beta-chain, mAb (52H10) is a monoclonal antibody that crossreacts with human protein. Works in ELISA, WB, IP. Important for Inflammation, Oxidative Stress, ROS, Immunology research.
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The assembly and activation of the early components of complement, after their interaction with antibody-antigen complexes, are described in terms of the structures of the different proteins taking part. C1q, a molecule of unique half collagen-half globular structure, binds to the second constant domain of the antibody molecules through its six globular heads. A tetrameric complex of C1r2-C1s2 binds to the collagenous tails and leads to formation of the serine-type proteases C1¯r and C1¯s. C1¯s activates C4, which forms a covalent bond between its α chain and the Fab section of the antibody. C2 is also activated by C1¯s and associates with the bound C4¯ molecule to form C42¯, a labile protease that activates C3, but which loses activity as the C2¯ peptide chains dissociate from C4¯. C2, by analogy with factor B, the equivalent component of the alternative pathway of activation, appears to be a novel type of serine protease with a similar catalytic site but different activation ...
Learn how uncontrolled or excessive complement activation may play a role in several autoimmune and inflammatory diseases, and why APL-2 (pegcetacoplan) targeting of complement proteins at the level of C3 is being investigated as a treatment.
While CRP can be an indicator of inflammation or infection, it is not always elevated when inflammation is present in the body. At the onset of an acute episode of inflammation, the CRP might be high. As the inflammation progresses to a chronic status, the CRP MAY go down though the inflammation is present. The reason for this is not known and is often seen in diseases like lupus and rheumatoid arthritis. In the body, CRP plays the important role of interacting with the complement system, an immunologic defense mechanism. C3 Complement and C4 Complements are often measured to get further indications of inflammation in the body ...
Date: 1906. : the process of binding serum complement to the product formed by the union of an antibody and the antigen for which it is specific that occurs when complement is.
Avhandlingar om COMPLEMENT ACTIVATION. Sök bland 90495 avhandlingar från svenska högskolor och universitet på Avhandlingar.se.
2004 (English)In: Proc Natl Acad Sci U S A, ISSN 0027-8424, Vol. 101, no 48, 16879-84 p.Article in journal (Refereed) Published ...
Fetal development inside the womb has many benefits, including protection from fluctuations in nourishment, temperature, and oxygen levels (41). Beyond the safety from external threats, fetal in utero existence, however, entails problems. Among the biggest challenges for mother and fetus is the establishment of immunologic coexistence of 2 genetically distinct entities while simultaneously ensuring potent immune defense against pathogens. To date, several maternal and fetal mechanisms contributing to the establishment and maintenance of fetal-maternal immune homeostasis have been described (11). Yet, numerous non-pathogen-related inflammatory reactions leading to pregnancy complications exist, which represent major threats to the developing fetus and its mother (42). Using a CMP-Sia-negative mouse model, we demonstrated sialylation to be crucial for protection of fetal extraembryonic tissue from maternal complement attack, thereby guaranteeing its proper development, which ultimately ensures ...
An immune-based approach to allow antibodies in the plasma of HIV-1-infected individuals to regain their activity of antibody-dependent complement-mediated lysis (2010 ...
... is an interesting technique that complements gene transfection and RNA interference for studying protein function and cellular pathways.
Learn about the signs, symptoms, and treatment of Complement 3 Deficiency, C3 Deficiency, and what to do if your dog has this health condition.
8. This allows further bacterial multi- plication topama subsequent production of an increased amount of inflammatory mediators via the complement system and other pathways.
Enzymes what would we do without them? Im guessing we probably die because we need them to sustain life! Ok we all know what an enzyme is, they are biological catalyst, which speed up a chemical reaction by providing an alternate pathway with a lower activation energy. The enzyme itself however is not used up,…
chr04:complement(join(34150379..34150670,34150237..34150289,34150030..34150153,34149819..34149940,34148628..34148735,34148427..34148528 ...
chr08:complement(join(8594165..8594329,8592744..8592818,8592340..8592396,8592099..8592259,8591848..8591988,8591180..8591282,8590996..8591095,8590688..8590899 ...
When I was growing up, the word cancer was a taboo word spoken in hushed tones. More often it was referred to as the big C.
Title: CH50: A Revisited Hemolytic Complement Consumption Assay for Evaluation of Nanoparticles and Blood Plasma Protein Interaction. VOLUME: 8 ISSUE: 3. Author(s):Ameena Meerasa, Jasper G. Huang and Frank X. Gu. Affiliation:Department of Chemical Engineering, University of Waterloo, 200 University Avenue West, Waterloo, ON N2L 3G1.. Keywords:CH50 assay, complement activation, hemolytic assay, nanoparticles, opsonization, protein interaction, stealth, toxicity, Plasma Protein, vasculature. Abstract: The use of nanoparticles as platforms or vehicles for applications in nanomedicine, such as drug delivery and medical imaging, has been widely reported in the literature. A key area of potential improvement in the development and implementation of nanoparticles is the design of surface treatments to maximize residence time in the bloodstream. Major obstacles to the prolonged circulation of nanoparticles include complement activation and opsonization, both of which contribute to the removal of foreign ...
A complement receptor is a receptor of the complement system, part of the innate immune system. Complement receptors bind proteins of the complement system, and can thus detect pathogens without mediation by antibodies. Complement activity is not antigen sensitive, but can be triggered by specific antigens. Many white blood cells express complement receptors on their surface, particularly monocytes and macrophages. All four complement receptors bind to fragments of complement component 3 or complement component 4 coated on pathogen surface, but the receptors have different functions. Complement receptor (CR) 1, 3, and 4 work as opsonins (stimulate phagocytosis), whereas CR2 is expressed only on B cells as a co-receptor. Red blood cells (RBCs) also express CR1. With these receptors, RBCs bring antigen-antibody complexes bound to complement fragments in the blood to the liver and spleen for degradation. Defects in these receptors can be associated with disease. Immune system Humoral immunity ...
Purpose: : Uncontrolled activation of the alternative complement pathway is thought to be associated with age-related macular degeneration (AMD). Previously, we have shown that in retinal pigmented epithelium (RPE) monolayers, oxidative stress reduced complement inhibitor expression and function on the cell surface, resulting in sublytic activation of the membrane attack complex . Here we examined the potential ligand and pathway(s) involved in initiating complement-dependent RPE cell damage by oxidative stress. Methods: : ARPE-19 cells were grown as monolayers on transwell plates. Sublytic complement activation was induced by challenging monolayers with H2O2 in the presence of complement-sufficient normal human serum (NHS). Since sublytic complement activation results in VEGF release, which in turn reduces barrier function, transepithelial electrical resistance (TER) measurements were used as a measure of cell injury. Results: : (1) TER deteriorated rapidly in H2O2-exposed monolayers upon ...
Whole hemolytic complement and three components (C1q, C4, and C3) were measured in pleural fluids obtained from 50 patients-23 with malignant disease, 6 with lupus erythematosus, 6 with rheumatoid arthritis, 3 with congestive heart failure, 3 with pulmonary embolism, and 9 in whom the cause of the pleural effusion was not ascertained. The mean values for whole complement and the three components were lowest in lupus erythematosus and rheumatoid arthritis patients. Compared with the malignant disease group, these differences were statistically significant (P , 0.01) for whole complement, C4, and C3. Anticomplementary activity was found in pleural fluids from some patients with lupus erythematosus or rheumatoid arthritis. This suggests that the pleural fluid complement depletion may be secondary to immunologic inactivation and that immune mechanisms may contribute to the development of Pleuritis in lupus erythematosus and rheumatoid arthritis. ...
Forty strains of Aeromonas hydrophila and Aeromonas veronii recovered from invasive and non-invasive infections were tested for their susceptibility to complement-mediated lysis by 65% pooled human serum (PHS). Based upon the results of this assay, two major populations could be defined. The first group (n = 20) consisted of serogroup 0:11 strains, all of which possessed a paracrystalline surface layer (S layer); all of these strains were refractory to the bactericidal activity of 65% PHS with the exception of A. hydrophila strain AH-121, which was composed of mixed subpopulations of serum-susceptible and serum-resistant clones. A second collection of isolates (n = 20), all of which were S-layer-negative, contained a subgroup of strains (n = 7) that were highly susceptible to complement-mediated lysis, showing a greater than 100-fold reduction of viable progeny within 30 min of exposure to 65% PHS. Serum-resistant strains from both groups could not be lysed by exposure of bacterial cells to polyclonal
Background/Purpose: The influence of complement-mediated innate immune responses on cartilage and bone homeostasis in the ageing joint have not been studied. Inappropriate complement-mediated cell damage is prevented by membrane regulators such as CD59. Synovial tissue expression of CD59 is altered during inflammatory arthritis; elevated CD59 levels may be necessary to protect joint tissues. Roles of CD59 in maintaining tissue equilibrium and structural architecture within the synovial joint have not been described previously. Since CD59a is the primary regulator of membrane attack complex assembly in mice; we used CD59a-gene-deleted mice (CD59a-/-) as tools to unravel the function of CD59a in modulating age-related joint degeneration. Methods: Hind limbs were collected from C57BL/6J wild type (WT) and CD59a-/- mice at 8-, 20- and 50- weeks of age (6 to 10 mice/group). The Mankin score was used to classify the histopathological severity of osteoarthritic (OA) lesions. Three dimensional ...
Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17621-6. doi: 10.1073/pnas.1003750107. Epub 2010 Sep 27. Research Support, N.I.H., Extramural; Research Support, U.S. Govt, Non-P.H.S.
Cerebral IR injury produces a profound inflammatory response characterized by neutrophil, macrophage, and platelet accumulation, upregulation of adhesion molecules, blood-brain barrier destruction, and cytokine production.5 During central nervous system inflammation, complement activation plays a direct role in neuronal cell death6 and has been implicated in many disease processes, including subarachnoid hemorrhage,9 Alzheimer disease,10 trauma,11 and stroke.12,13 In a study of patients who died after ischemic stroke, Lindsberg et al9 demonstrated complement deposition within areas of necrosis and concluded that activation of the terminal complement pathway with membrane attack complex assembly occurs within cerebral infarct zones. Others have shown that complement depletion before cerebral IR injury may have neuroprotective effects in animal models.12,14 Huang et al12 used a mouse model of middle cerebral artery occlusion and reperfusion to demonstrate that administering a potent inhibitor of ...
AMYNDAS is developing a novel peptidic complement inhibitor AMY-101, based on the third-generation compstatin analogue Cp40. AMY-101 is a selective inhibitor of complement activation in humans and in NHP. It binds to the complement component C3, the central functional hub that controls the upstream activation/amplification and downstream effector functions of complement. By binding to C3, AMY-101 inhibits the cleavage of native C3 to its active fragments C3a and C3b. As a consequence, the deposition of C3b, amplification via the alternative pathway and all downstream complement responses are prevented. AMY-101 is being developed to treat complement-mediated diseases, which are largely driven by aberrant C3 activation.. This first-in-human study of the C3-targeting complement inhibitor AMY-101 investigates the safety and PK/PD profile of AMY-101 in healthy male volunteers after Single Ascending Dose (SAD) and Multiple Doses (MD) using subcutaneous (SQ) or intravenous (IV) administration. The ...
Lipooligosaccharide (LOS) heptose (Hep) glycan substitutions influence gonococcal serum resistance. Several gonococcal strains bind the classical complement pathway inhibitor, C4b-binding protein (C4BP), via their porin (Por) molecule to escape complement-dependent killing by normal human serum (NHS). We show that the proximal glucose (Glc) on HepI is required for C4BP binding to Por1B-bearing gonococcal strains MS11 and 1291 but not to FA19 (Por1A). The presence of only the proximal Glc on HepI (lgtE mutant) permitted maximal C4BP binding to MS11 but not to 1291. Replacing 1291 lgtE Por with MS11 Por increased C4BP binding to levels that paralleled MS11 lgtE, suggesting that replacement of the Por1B molecule dictated the effects of HepI glycans on C4BP binding. The remainder of the strain background did not affect C4BP binding; replacing the Por of strain F62 with MS11 Por (F62 PorMS11) and truncating HepI mirrored the findings in the MS11 background. C4BP binding correlated with resistance to killing
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 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 ...
OP28 The complement component C3 is expressed by the endometrial ectopic tissue and is involved in the endometriotic lesion formation C. Agostinis 1, G. Zito 1, D. De Santo1, R. Vidergar2, O. Radillo 1, F. Bossi 1, S. Zorzet2, G. Ricci 1, R. Bulla 2 1 Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy 2 Department of Life Sciences, University of Trieste, Trieste, Italy E-mail address: [email protected] (C. Agostinis). Background: The complement (C) system is one of the major components of humoral innate immunity, acting as the first lines of defence against microbes. The principal roles of C system are the opsonization and lysis of pathogens, but new roles in inflammatory and immunological processes are emerging. It is involved in numerous inflammatory diseases, such as SLE, PNH and endometriosis (EM). Several groups have been demonstrated that the glandular epithelial cells found in endometriotic implants produce and secrete the C component C3. The aim ...
BACKGROUND AND OBJECTIVES: Inherited complement hyperactivation is critical for the pathogenesis of atypical hemolytic uremic syndrome (HUS) but undetermined in postdiarrheal HUS. Our aim was to investigate complement activation and variants of complement genes, and their association with disease severity in children with Shiga toxin-associated HUS. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Determination of complement biomarkers levels and next-generation sequencing for the six susceptibility genes for atypical HUS were performed in 108 children with a clinical diagnosis of post-diarrheal HUS (75 Shiga toxin-positive, and 33 Shiga toxin-negative) and 80 French controls. As an independent control cohort, we analyzed the genotypes in 503 European individuals from the 1000 Genomes Project. RESULTS: During the acute phase of HUS, plasma levels of C3 and sC5b-9 were increased, and half of patients had decreased membrane cofactor protein expression, which normalized after 2 weeks. Variants with minor
Objective: Complement proteins have been associated with atherosclerosis and cardiovascular risk factors. Recent data suggest a potential role of complement protein C3 in clot stability with hypofibrinolytic and prothrombotic features. Women after menopause are at greater risk of cardiovascular disease and have significantly higher levels of C3 compared with younger women. To better understand the association between complement proteins and atherosclerosis we evaluated the cross-sectional associations between complement proteins C3 and C4 and hemostatic markers (factor VIIc, fibrinogen, plasminogen activator inhibitor-1 (PAI-1) antigen and tissue plasminogen activator (tPA) antigen) in a sample of midlife women.. Design: Pilot data from the Study of Womens Health Across the Nation (SWAN) Pittsburgh site were used. Both C3 and C4 were measured using frozen serum specimens by immunoturbidimetric assay. Data for hemostatic markers were available in SWAN Core data (factor VIIc and fibrinogen were ...

MBL2 gene - Genetics Home ReferenceMBL2 gene - Genetics Home Reference

This binding turns on (activates) the complement system, which is a group of immune system proteins that work together to ... This protein complex plays an important role in the immune systems response to foreign invaders (pathogens). ... The MBL2 gene provides instructions for making a protein that assembles into a protein complex called mannose-binding lectin. ... leading to a decreased number of subunits available for protein assembly and a reduction in the amount of functional protein. ...
more infohttps://ghr.nlm.nih.gov/gene/MBL2

Molecular cloning and chromosomal localization of human membrane cofactor protein (MCP). Evidence for inclusion in the...Molecular cloning and chromosomal localization of human membrane cofactor protein (MCP). Evidence for inclusion in the...

Membrane cofactor protein (MCP), a regulatory molecular of the complement system with cofactor activity for the factor I- ... C4-binding protein, and factor H), as well as several other complement and non-complement proteins. The remainder of the MCP ... The deduced full-length MCP protein consists of a 34-amino acid signal peptide and a 350-amino acid mature protein. The protein ... Complement-mediated tumor cell damage induced by antibodies against membrane cofactor protein (MCP, CD46). ...
more infohttps://rupress.org/jem/article/168/1/181/49547/Molecular-cloning-and-chromosomal-localization-of

Structural and functional characterization of human and murine C5a anaphylatoxins (Journal Article) | SciTech ConnectStructural and functional characterization of human and murine C5a anaphylatoxins (Journal Article) | SciTech Connect

Complement is an ancient part of the innate immune system that plays a pivotal role in protection against invading pathogens ... Whereas A8{sup Δ71-73} adopts a three-helix bundle conformation similar tomore » human C5a-desArg, the two murine proteins form ... Upon complement activation, a cascade of proteolytic events generates the complement effectors, including the anaphylatoxins ... Signalling through their cognate G-protein coupled receptors, C3aR and C5aR, leads to a wide range of biological events ...
more infohttps://www.osti.gov/scitech/biblio/22347767-structural-functional-characterization-human-murine-c5a-anaphylatoxins

Sars Internal: Sars Seminar AbstractsSars Internal: Sars Seminar Abstracts

However, ribosomal protein genes are notable exceptions as the majority of them appear as 2-6 gene clusters in the same operons ... This is indispensable for the future of this model system here but also to be able to export it toward other institutes. We ... dioica has evolved its gene complement to adapt to these processes and their transitions (e.g. specific gene variants). As an ... Sprouty proteins are an important group of RTK inhibitors. Sprouty 1 is expressed in several signaling centers during ...
more infohttp://www.sars.no/internal/secure/news/abstracts2006.php

Complement System Proteins
      - Complement
     Summary | CureHunter MobileComplement System Proteins - Complement Summary | CureHunter Mobile

Also Known As: Complement; Complement, Hemolytic; Complement Protein; Protein, Complement; Proteins, Complement System Show All ... Complement System Proteins (Complement) Summary Description: Serum glycoproteins participating in the host defense mechanism of ... Key Diseases for which Complement System Proteins is Relevant. * Infection : 87 outcomes 156 studies in 2347 results ... CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).. ...
more infohttp://www.curehunter.com/m/keywordSummaryD003165.do

Complement System Proteins - Semantic ScholarComplement System Proteins - Semantic Scholar

This complement system consists of three separate activation triggers: (1) Ab binding to a cell surface, (2) formation of ... The complement system is a complex system of serum proteins that interact in a cascade. Many of the early components are serine ... Complement System Proteins. Known as: Proteins, Complement System, Complement, Complement Component Protein (More). ... The complement system is a complex system of serum proteins that interact in a cascade. Many of the early components are serine ...
more infohttps://www.semanticscholar.org/topic/Complement-System-Proteins/1546

WHO HQ Library catalog ›

    Results of search for su:{Complement system proteins}WHO HQ Library catalog › Results of search for 'su:{Complement system proteins}'

Results of search for su:{Complement system proteins} Refine your search. *Availability * Limit to currently available items. ... Complement and infectious diseases / author, Douglas P. Fine.. by Fine, Douglas P ...
more infohttps://kohahq.searo.who.int/cgi-bin/koha/opac-search.pl?q=su:%7BComplement%20system%20proteins%7D

INTERACTIONS OF C-REACTIVE PROTEIN WITH THE COMPLEMENT SYSTEM | JEMINTERACTIONS OF C-REACTIVE PROTEIN WITH THE COMPLEMENT SYSTEM | JEM

INTERACTIONS OF C-REACTIVE PROTEIN WITH THE COMPLEMENT SYSTEM. Joan Siegel, Rosemarie Rent, Henry Gewurz ... We conclude that CRP is a potent activator of the C system at the level of C1, and that polycations such as protamine sulfate ... It seems not unlikely that one role of CRP in health and disease involves its ability to interact with the C system. ... It was mediated by a heat-stable nondialyzable factor which separated with C-reactive protein (CRP) during fractionation and ...
more infohttp://jem.rupress.org/content/140/3/631

Protein that foils complement system may be key to smallpox virulence | CIDRAPProtein that foils complement system may be key to smallpox virulence | CIDRAP

... smallpox virus has a protein that inhibits the human complement system far more effectively than does its counterpart protein ... in the closely related vaccinia virus, used in smallpox vaccine, according to researchers who compared the two proteins. This ... Protein that foils complement system may be key to smallpox virulence. Filed Under: ... Jun 10, 2002 (CIDRAP News) The smallpox virus has a protein that inhibits the human complement system far more effectively than ...
more infohttp://www.cidrap.umn.edu/news-perspective/2002/06/protein-foils-complement-system-may-be-key-smallpox-virulence

Membrane cofactor protein of the complement system: alternative splicing of serine/threonine/proline-rich exons and cytoplasmic...Membrane cofactor protein of the complement system: alternative splicing of serine/threonine/proline-rich exons and cytoplasmic...

Membrane cofactor protein of the complement system: alternative splicing of serine/threonine/proline-rich exons and cytoplasmic ... Membrane cofactor protein of the complement system: alternative splicing of serine/threonine/proline-rich exons and cytoplasmic ... Membrane cofactor protein (MCP) is a complement regulatory protein that is expressed on human cells and cell lines as two ... indicated that MCP was a type 1 membrane glycoprotein and a member of the regulators of complement activation gene/protein ...
more infohttp://jem.rupress.org/content/174/1/93

Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures |...Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures |...

Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures. S J ... Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures ... Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures ... Identity of the putative serine-proteinase fold in proteins of the complement system with nine relevant crystal structures ...
more infohttp://www.biochemj.org/content/295/1/109

Complement Component / Protein of Complement SystemComplement Component / Protein of Complement System

Protein of Complement System.The activated complement system recognizes and eliminates invading microorganisms and thus is ... Complement Component / Protein of Complement System. Complement Component / Protein of Complement System ... Complement Regulator of Complement System: Membrane Cofactor Protein / MCP / CD46. *Complement Regulator of Complement System: ... More Complement Component / Protein of Complement System Complement Component Factor B/CFB products: proteins, antibodies, ...
more infohttps://kr.sinobiological.com/complement-component-protein-of-complement-system-lgf.html

Complement resistance in Branhamella (Moraxella) catarrhalis.  - PubMed - NCBIComplement resistance in Branhamella (Moraxella) catarrhalis. - PubMed - NCBI

Complement System Proteins/immunology*. *Humans. *Moraxella catarrhalis/immunology*. *Neisseriaceae Infections/microbiology. ... Complement resistance in Branhamella (Moraxella) catarrhalis.. Hol C, Verduin CM, van Dijke E, Verhoef J, van Dijk H. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/8098421?dopt=Abstract

The Effect of Some Drugs Used in Treatment of Vasculitis on the Complement System in Children - Full Text View - ClinicalTrials...The Effect of Some Drugs Used in Treatment of Vasculitis on the Complement System in Children - Full Text View - ClinicalTrials...

Complement System Proteins. Methylprednisolone. Abortifacient Agents, Nonsteroidal. Abortifacient Agents. Reproductive Control ... The Effect of Some Drugs Used in Treatment of Vasculitis on the Complement System in Children. The safety and scientific ... The Effect of Some Drugs Used in Treatment of Vasculitis on the Complement System in Children Attending Assiut University ... Complement activation at C3 and C4 was involved in organ damage, especially renal, in AAV at the alternative complement pathway ...
more infohttps://www.clinicaltrials.gov/ct2/show/NCT03692416?term=vasculitis&

Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...

Immune System Diseases. Complement System Proteins. Autoantibodies. Immunologic Factors. Physiological Effects of Drugs. ... Change in complement levels between groups from baseline to week 12. *change in complement levels 2 [ Time Frame: up to 52 ... Complement levels elevation [ Time Frame: up to 52 weeks ]. Evaluation of complement levels at study entry to determine which ... Normalisation of complement activation [ Time Frame: up to 52 weeks ]. Normalization of complement activation at 4 weeks, 8, 12 ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01275287?recr=Open&cond=%22Vasculitis%22&rank=6

Network Analysis of Urinary Molecular Signature Complements Clinical Data to Predict Postoperative Acute Kidney Injury - Full...Network Analysis of Urinary Molecular Signature Complements Clinical Data to Predict Postoperative Acute Kidney Injury - Full...

Change in urine protein biomarkers (urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of ... Change in urine protein biomarkers (urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of ... Change from baseline in urine protein biomarkers at 4 hours after surgery [ Time Frame: Baseline, 4 hours after surgery ]. ... Change from baseline in urine protein biomarkers at postoperative day 1 [ Time Frame: Baseline, day 1 after surgery ]. ...
more infohttps://www.clinicaltrials.gov/ct2/show/NCT02114138

Eculizumab Therapy for Chronic Complement-Mediated Injury in Kidney Transplantation - Full Text View - ClinicalTrials.govEculizumab Therapy for Chronic Complement-Mediated Injury in Kidney Transplantation - Full Text View - ClinicalTrials.gov

complement protein. eculizumab. Kidney transplantation. Additional relevant MeSH terms: Complement System Proteins. Immunologic ... Eculizumab is an antibody that has been developed to inhibit the complement protein C5. Eculizumab will be delivered via IV ... Eculizumab Therapy for Chronic Complement-Mediated Injury in Kidney Transplantation. The safety and scientific validity of this ... Number of circulating endothelial cells with evidence of injury and bound antibody and/or complement [ Time Frame: baseline, 3, ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01327573

CFH haplotypes without the Y402H coding variant show strong association with susceptibility to age-related macular degeneration...CFH haplotypes without the Y402H coding variant show strong association with susceptibility to age-related macular degeneration...

A common polymorphism, encoding the sequence variation Y402H in complement factor H (CFH), has been strongly associated with ... Molecular Mechanisms of Complement System Proteins and Matrix Metalloproteinases in the Pathogenesis of Age-Related Macular ... Association Between Complement FactorC2/C3/CFB/CFHPolymorphisms and Age-Related Macular Degeneration: A Meta-Analysis *Feiteng ... Two distinct conformations of factor H regulate discrete complement-binding functions in the fluid phase and at cell surfaces * ...
more infohttps://www.nature.com/articles/ng1871?error=cookies_not_supported&code=232d8696-8564-439c-8bc3-5b814b41a61f

Complement-dependent and -independent pathways of T cell-B cell cooperation.Complement-dependent and -independent pathways of T cell-B cell cooperation.

Complement C3 / analysis, antagonists & inhibitors. Complement System Proteins*. Cytotoxicity Tests, Immunologic. Erythrocytes ... 0/Antibodies; 0/Antigens; 0/Complement C3; 0/Immunoglobulin M; 0/Snake Venoms; 0/Trinitrobenzenes; 9007-36-7/Complement System ...
more infohttp://www.biomedsearch.com/nih/Complement-dependent-independent-pathways-T/323359.html

Immunological study of vulvar lichen sclerosus: preliminary considerations.Immunological study of vulvar lichen sclerosus: preliminary considerations.

Complement System Proteins / analysis*. Female. Humans. Immunoglobulins / blood*. Lymphocyte Subsets / pathology*. Middle Aged ... 0/Autoantibodies; 0/Immunoglobulins; 9007-36-7/Complement System Proteins From MEDLINE®/PubMed®, a database of the U.S. ...
more infohttp://www.biomedsearch.com/nih/Immunological-study-vulvar-lichen-sclerosus/8471134.html

Complement proteins Protocols and Video ArticlesComplement proteins Protocols and Video Articles

Label-Free Imaging of Single Proteins Secreted from Living Cells via iSCAT Microscopy, High Yield Expression of Recombinant ... A Convenient and General Expression Platform for the Production of Secreted Proteins from Human Cells, Simplified Reverse ... Conjugative Mating Assays for Sequence-specific Analysis of Transfer Proteins Involved in Bacterial Conjugation. ... Human Proteins with the Transient Transfection of HEK293 Cells in Suspension, ...
more infohttps://www.jove.com/search?q=complement%20proteins

Nyremedicin (Nefrologi) - Publications
     - Aalborg Universitys Research PortalNyremedicin (Nefrologi) - Publications - Aalborg University's Research Portal

High levels of urinary complement proteins are associated with chronic renal damage and proximal tubule dysfunction in ...
more infohttps://vbn.aau.dk/en/organisations/nyremedicin-nefrologi-2/publications/

Search | IOVS | ARVO JournalsSearch | IOVS | ARVO Journals

TAGS: adenovirus infections, adenoviruses, antigens, cd55, complement system proteins, complement membrane attack complex, age- ... CD46, CD55, And CD59-mediated Attenuation Of Complement-induced Damage On Murine RPE Cells In-vitro And In-vivo: Therapeutic ... Decay Accelerating Factor (CD55)-Mediated Attenuation of Complement: Therapeutic Implications for Age-Related Macular ...
more infohttps://iovs.arvojournals.org/solr/searchresults.aspx?author=Kelly+N.+Ma

Letter from Michael Heidelberger to Enrique E. Ecker, Western Reserve University  (April 24, 1945)Letter from Michael Heidelberger to Enrique E. Ecker, Western Reserve University (April 24, 1945)

Complement System Proteins Exhibit Category: Antigens and Antibodies: Heidelberger and The Rise of Quantitative Immunochemistry ... He proved that complement was made up of a group of specific chemical substances that could be isolated in the laboratory, and ... and guinea pig complement. The letter illustrates Heidelbergers role as arbitrator, critic, and guardian of a uniform ... the only two of our complement team left, will fight it out until some agreement is reached. Otherwise, I fear the same ...
more infohttps://profiles.nlm.nih.gov/ps/retrieve/ResourceMetadata/DHBBGJ

Participants at the National Academy of Sciences Conference on Complement] [1950]Participants at the National Academy of Sciences Conference on Complement] [1950]

Complement System Proteins Exhibit Category: Antigens and Antibodies: Heidelberger and The Rise of Quantitative Immunochemistry ... National Academy of Sciences Conference on Complement (March 1951) Box Number: 4. Folder Number: 10. Unique Identifier: DHBBMZ ... Participants at the National Academy of Sciences Conference on Complement]. High resolution version (8,264,364 Bytes) ... This photograph is of attendees at an interdisciplinary conference on complement organized by Heidelberger (9th from the left) ...
more infohttps://profiles.nlm.nih.gov/ps/retrieve/ResourceMetadata/DHBBMZ
  • Because SPICE efficiently inhibits the stability of human C3b and C4b, it essentially inactivates the convertases and, therefore, both the classical and alternative pathways of complement," the report says. (umn.edu)
  • Complement Factor D at the US National Library of Medicine Medical Subject Headings (MeSH) This article incorporates text from the United States National Library of Medicine, which is in the public domain. (wikipedia.org)
  • He proved that complement was made up of a group of specific chemical substances that could be isolated in the laboratory, and that it had essential functions in activating host defense mechanisms against invading microorganisms. (nih.gov)
  • 5 More than 30 proteins act synergically to provide host defense against cells, microorganisms, and tissues identified as abnormal by a specific antibody. (scielo.br)
  • Here, we identify a kidney-specific anatomical and functional unit, formed by resident macrophages and peritubular capillary endothelial cells, which monitors the transport of proteins and particles ranging from 20 to 700 kDa or 10 to 200 nm into the kidney interstitium. (bireme.br)
  • Recombinant SPICE and VCP proteins then were produced in mammalian and insect cells. (umn.edu)
  • The expression in a single cell of four distinct protein species with variable STP-rich regions and cytoplasmic tails represents an interesting example of the use of alternative splicing to provide variability in a mammalian protein. (rupress.org)
  • A common polymorphism, encoding the sequence variation Y402H in complement factor H (CFH), has been strongly associated with disease susceptibility. (nature.com)
  • The letter illustrates Heidelberger's role as arbitrator, critic, and guardian of a uniform terminology in the new field of complement chemistry, a field Heidelberger helped launch in the late 1930s and early 1940s. (nih.gov)
  • This photograph is of attendees at an interdisciplinary conference on complement organized by Heidelberger (9th from the left) and held June 12 to 15, 1950, on Shelter Island, New York. (nih.gov)
  • Monoclonal gammopathy of undetermined significance Primary AL amyloidosis (light chains only) These are characterized by the presence of any abnormal protein that is involved in the immune system, which are most often immunoglobulins and are associated with the clonal proliferation of lymphocytes. (wikipedia.org)
  • Paraproteinemias may be categorized according to the type of monoclonal protein found in blood:[citation needed] Light chains only (or Bence Jones protein). (wikipedia.org)
  • In this case, the paraprotein goes under the name of "M-protein" ("M" for monoclonal). (wikipedia.org)
  • Complement and infectious diseases / author, Douglas P. Fine. (who.int)
  • In addition to this, several other drivers of the global immunoprotein diagnostic testing market comprises of awareness among population towards early diagnosis, well- established healthcare systems and the rise in incidence of infectious diseases in the developing countries due to unhygienic conditions. (coherentmarketinsights.com)
  • Jun 10, 2002 (CIDRAP News) The smallpox virus has a protein that inhibits the human complement system far more effectively than does its counterpart protein in the closely related vaccinia virus, used in smallpox vaccine, according to researchers who compared the two proteins. (umn.edu)
  • It seems not unlikely that one role of CRP in health and disease involves its ability to interact with the C system. (rupress.org)
  • Complement is one of the first lines of defence in innate immunity and is important for cellular integrity, tissue homeostasis and modifying the adaptive immune response. (sinobiological.com)
  • The individual complement reactions develop in a sequential manner, allowing regulation that modulates the intensity of the response and adjusts the effector functions for the specific immune response. (sinobiological.com)
  • Human complement levels are known to reflect the presence of clinical infection, with low levels indicative of increased utilization in the body's immune response. (biomedsearch.com)
  • An integrated view of the roles and mechanisms of heat shock protein gp96-peptide complex in eliciting immune response. (elsevier.com)
  • In addition, complement facilitates the elimination of dead or modified self cells, such as apoptotic particles and cellular debris. (sinobiological.com)
  • The fact that SPICE functions better against human complement quantitatively and qualitatively demonstrates that variola exhibits human preference at the protein level, a concept previously suggested, but not shown," the report states. (umn.edu)
  • Complement C3a enhances CXCL12 (SDF-1)-mediated chemotaxis of bone marrow hematopoietic cells independently of C3a receptor. (harvard.edu)
  • These proteins possess an immunological activity against pathogenic organisms and substances as they display an abnormal increase in blood concentration thereby acting as a potential indicator in disease diagnosis during an unhealthy state. (coherentmarketinsights.com)
  • Complement Receptor 2 is increased in cerebrospinal fluid of multiple sclerosis patients and regulates C3 function. (semanticscholar.org)
  • Even patients with severe movement dysfunction can benefit from intensive exercise practice as the TUTOR system picks up even small angles of joint movement. (wordpress.com)
  • Analysis by polymerase chain reaction, Northern blots, and transfection indicated that the predominance of MCP cDNA isoforms with STPB correlated with the high molecular weight protein phenotype, while the predominance of isoforms without STPB correlated with the lower molecular weight phenotype. (rupress.org)