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.
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.
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).
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.
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.
A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.
Complement 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.
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.
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.
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.
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.
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.
Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.
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.
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.
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).
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.
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).
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).
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).
Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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 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.
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.
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)
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.
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.
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.
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.
A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.
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.
Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.
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.
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.
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.
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.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
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.
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.
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.
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.
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.
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).
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.
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.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
A derivative of complement C5a, generated when the carboxy-terminal ARGININE is removed by CARBOXYPEPTIDASE B present in normal human serum. C5a des-Arg shows complete loss of spasmogenic activity though it retains some chemotactic ability (CHEMOATTRACTANTS).
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.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
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.
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.
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.
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.
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.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
Antibodies produced by a single clone of cells.
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).
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.
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.
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.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
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.
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.
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.
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.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
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.
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.
The clear portion of BLOOD that is left after BLOOD COAGULATION to remove BLOOD CELLS and clotting proteins.
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.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
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.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Polysaccharides consisting of mannose units.
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.
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.
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.
A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.
A metallocarboxypeptidase that removes C-terminal basic amino acid from peptides and proteins, with preference shown for lysine over arginine. It is a plasma zinc enzyme that inactivates bradykinin and anaphylatoxins.
Amyloid P component is a small, non-fibrillar glycoprotein found in normal serum and in all amyloid deposits. It has a pentagonal (pentaxin) structure. It is an acute phase protein, modulates immunologic responses, inhibits ELASTASE, and has been suggested as an indicator of LIVER DISEASE.
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.
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.
Proteins prepared by recombinant DNA technology.
A specific immune response elicited by a specific dose of an immunologically active substance or cell in an organism, tissue, or cell.
Inflammation of any part of the KIDNEY.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.
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.
The COOH-terminal fragment of COMPLEMENT 2, released by the action of activated COMPLEMENT C1S. It is a SERINE PROTEASE. C2a combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
Immunoelectrophoresis in which a second electrophoretic transport is performed on the initially separated antigen fragments into an antibody-containing medium in a direction perpendicular to the first electrophoresis.
Visible accumulations of fluid within or beneath the epidermis.
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.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
A chronic and relatively benign subepidermal blistering disease usually of the elderly and without histopathologic acantholysis.
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.
Infections with bacteria of the species NEISSERIA MENINGITIDIS.
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.
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.
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.
Glycoproteins found on the membrane or surface of cells.
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.
Modified oligonucleotides in which one of the oxygens of the phosphate group is replaced with a sulfur atom.
A type of glomerulonephritis that is characterized by the accumulation of immune deposits (COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane.
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
Transport proteins that carry specific substances in the blood or across cell membranes.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
A species of gram-negative, aerobic BACTERIA. It is a commensal and pathogen only of humans, and can be carried asymptomatically in the NASOPHARYNX. When found in cerebrospinal fluid it is the causative agent of cerebrospinal meningitis (MENINGITIS, MENINGOCOCCAL). It is also found in venereal discharges and blood. There are at least 13 serogroups based on antigenic differences in the capsular polysaccharides; the ones causing most meningitis infections being A, B, C, Y, and W-135. Each serogroup can be further classified by serotype, serosubtype, and immunotype.
The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.
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.
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).
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
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.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
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)
Established cell cultures that have the potential to propagate indefinitely.
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.
An iron-binding protein that was originally characterized as a milk protein. It is widely distributed in secretory fluids and is found in the neutrophilic granules of LEUKOCYTES. The N-terminal part of lactoferrin possesses a serine protease which functions to inactivate the TYPE III SECRETION SYSTEM used by bacteria to export virulence proteins for host cell invasion.
Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.
All blood proteins except albumin ( = SERUM ALBUMIN, which is not a globulin) and FIBRINOGEN (which is not in the serum). The serum globulins are subdivided into ALPHA-GLOBULINS; BETA-GLOBULINS; and GAMMA-GLOBULINS on the basis of their electrophoretic mobilities. (From Dorland, 28th ed)
Local surface sites on antibodies which react with antigen determinant sites on antigens (EPITOPES.) They are formed from parts of the variable regions of FAB FRAGMENTS.
The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IMMUNOGLOBULIN G whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Elements of limited time intervals, contributing to particular results or situations.
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.
Crystallizable fragments composed of the carboxy-terminal halves of both IMMUNOGLOBULIN HEAVY CHAINS linked to each other by disulfide bonds. Fc fragments contain the carboxy-terminal parts of the heavy chain constant regions that are responsible for the effector functions of an immunoglobulin (COMPLEMENT fixation, binding to the cell membrane via FC RECEPTORS, and placental transport). This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
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.)
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
Methods used by pathogenic organisms to evade a host's immune system.
Proteins found in any species of bacterium.
The single layer of pigment-containing epithelial cells in the RETINA, situated closely to the tips (outer segments) of the RETINAL PHOTORECEPTOR CELLS. These epithelial cells are macroglia that perform essential functions for the photoreceptor cells, such as in nutrient transport, phagocytosis of the shed photoreceptor membranes, and ensuring retinal attachment.
A blood plasma glycoprotein that mediates cell adhesion and interacts with proteins of the complement, coagulation, and fibrinolytic cascade. (From Segen, Dictionary of Modern Medicine, 1992)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Synthetic or natural materials, other than DRUGS, that are used to replace or repair any body TISSUES or bodily function.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
Failure in built environment with loss of functional integrity.
An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.
Failure of the PLACENTA to deliver an adequate supply of nutrients and OXYGEN to the FETUS.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
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.

Up-regulated production and activation of the complement system in Alzheimer's disease brain. (1/1999)

We used reverse transcriptase-polymerase chain reaction and Western blotting techniques to measure the levels of complement mRNAs and their protein products in Alzheimer's disease (AD) brain compared with non-AD brain. mRNAs for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 were detected in the 11 regions of brain that were investigated. The mRNA levels were markedly up-regulated in affected areas of AD brain. In the entorhinal cortex, hippocampus, and midtemporal gyrus, which had dense accumulations of plaques and tangles, C1q mRNA was increased 11- to 80-fold over control levels, and C9 mRNA 10- to 27-fold. These levels were substantially higher than in the livers of the same cases. Western blot analysis of AD hippocampus established the presence of all of the native complement proteins as well as their activation products C4d, C3d, and the membrane attack complex. These data indicate that high levels of complement are being produced in affected areas of AD brain, that full activation of the classical complement pathway is continuously taking place, and that this activation may be contributing significantly to AD pathology.  (+info)

Capsular sialic acid limits C5a production on type III group B streptococci. (2/1999)

The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.  (+info)

Polymerization of IgA and IgM: roles of Cys309/Cys414 and the secretory tailpiece. (3/1999)

We have investigated how the secretory tailpiece (tp), Cys414 and the amino acids flanking Cys414 or Cys309 are involved in regulating the different polymerization of IgM and IgA to pentamers and dimers/monomers, respectively. Whereas changing the tp of IgM to that of IgA has little effect on IgM polymerization, introducing the mu tp to IgA leads to the formation of larger than wild-type IgA polymers, including pentamers and hexamer. This shows that the secretory tp can differentially regulate polymerization depending on the heavy chain context. Cys414, which is engaged in intermonomeric disulfide bonds in IgM, is not crucial for the difference in IgM and IgA polymerization; IgM with a C414S mutation forms more large polymers than IgA. Also, IgA with IgM-like mutations in the five amino acids flanking Cys309, which is homologous to Cys414, oligomerize similarly as IgA wild type. Thus, IgA appears to have an inherent tendency to form monomers and dimers that is partially regulated by the tp, while the Cys309 region has only a minor effect. We also show that complement activation by IgM is sensitive to alterations in the polymeric structure, while IgA is inactive in classical complement activation even for polymers such as pentamers and hexamers.  (+info)

Two constituents of the initiation complex of the mannan-binding lectin activation pathway of complement are encoded by a single structural gene. (4/1999)

Mannan-binding lectin (MBL) forms a multimolecular complex with at least two MBL-associated serine proteases, MASP-1 and MASP-2. This complex initiates the MBL pathway of complement activation by binding to carbohydrate structures present on bacteria, yeast, and viruses. MASP-1 and MASP-2 are composed of modular structural motifs similar to those of the C1q-associated serine proteases C1r and C1s. Another protein of 19 kDa with the same N-terminal sequence as the 76-kDa MASP-2 protein is consistently detected as part of the MBL/MASP complex. In this study, we present the primary structure of this novel MBL-associated plasma protein of 19 kDa, MAp19, and demonstrate that MAp19 and MASP-2 are encoded by two different mRNA species generated by alternative splicing/polyadenylation from one structural gene.  (+info)

Role of antibody and complement in opsonization of group B streptococci. (5/1999)

A requirement for the classic complement pathway in opsonization of group B streptococci was observed by using both a chemiluminescence and a radiolabeled bacterial uptake technique. The classic pathway increased levels of opsonization for types Ia and II stock and wild strains and for some type III wild strains. In contrast, other type III wild strains and the type III stock strain had accelerated kinetics of uptake in the presence of an intact classic pathway, but the level of opsonization was unchanged from that with antibody alone. We could not demonstrate a significant role for the alternative pathway in opsonizing stock or wild strains of group B streptococci. Futhermore, electrophoretic and complement consumption analysis by hemolytic titration failed to reveal alternative pathway activation by the majority of strains of this group. Therapy aimed at supplying opsonins for these organisms will require the presence of type-specific antibody.  (+info)

Anti-endothelial cell antibodies in systemic vasculitis and systemic lupus erythematosus (SLE): effects of heat inactivation on binding and specificity. (6/1999)

Heating sera is used to inactivate complement but may affect the binding characteristics of autoantibodies. We studied the effect of heating sera from patients with systemic vasculitides and SLE on antibody binding to cultured human umbilical vein endothelial cells. Sera from 32 patients with systemic vasculitides, eight with SLE and 10 healthy controls were studied for anti-endothelial cell antibodies (AECA) using an ELISA before and after heating sera to 56 degrees C for 30 min. The median (range) AECA binding index in the patient group increased from 20% (0-153%) to 71.5% (10-259%) (P < 0.0001). The AECA binding index in the control group also increased from 14% (0-52%) to 90% (42-154%) (P < 0.0001). The increased binding was unaffected by the addition of fresh complement or removal of immune complexes and the increased binding after heating persisted even after cooling to 4 degrees C. Specificity experiments showed that after heating, the binding specificity of sera was lost. Removal of immunoglobulin with Protein A abolished the increased binding seen after heating. Heating sera increases AECA binding in both patient and control sera. The mechanism is probably non-specific damage to the immunoglobulin molecule, and heating sera should thus be avoided.  (+info)

Influence of dialysis with polyamide vs haemophan haemodialysers on monokines and complement activation during a 4-month long-term study. (7/1999)

BACKGROUND: Contact between blood and dialysis membranes activates mononuclear cells and the complement system. The extent of activation is dependent on the dialyser material used and is considered an index of biocompatibility. Polyamide dialysers consist of a synthetic membrane that claims high standards of biocompatibility. Haemophan dialysers represent membranes made of modified cellulose that are now broadly used for treatment in Europe and are already considered to be more biocompatible than the cuprophane membranes that were used as reference in most previous studies. METHODS: In a cross-over treatment study short-term as well as long-term effects of a polyamide dialyser with respect to monokine induction and complement activation were compared to a haemophan dialyser. RESULTS: Neither haemophan nor polyamide dialysers induced relevant changes in plasma monokine levels. However, in vitro challenge of mononuclear cells with lipopolysaccharide (LPS) unmasked a significantly stronger preactivation for the secretion of proinflammatory monokines during haemophan than polyamide dialysis. Unlike other monokines the production of the regulatory monokine IL-10 was mainly influenced by individual factors and correlated with the patient's immune status rather than the dialyser type used. Enhanced preactivation of monocytes in haemophan compared to polyamide dialysis was paralleled by an increased complement activation. Cellular preactivation and formation of terminal complement complex remained constant over the 4-month treatment period. CONCLUSIONS: Haemophan and polyamide dialysers do not induce changes in plasma cytokine levels both during short-term and long-term use. However, they significantly differ in complement activation as well as preactivation of monocytes. Preactivated monocytes are prone to secrete high amounts of proinflammatory cytokines when exposed to a second stimulus like endotoxin. Secretion of the regulatory cytokine IL-10 is not influenced by the dialyser type.  (+info)

Recombinant glycoproteins that inhibit complement activation and also bind the selectin adhesion molecules. (8/1999)

Soluble human complement receptor type 1 (sCR1, TP10) has been expressed in Chinese hamster ovary (CHO) DUKX-B11 cells and shown to inhibit the classical and alternative complement pathways in vitro and in vivo. A truncated version of sCR1 lacking the long homologous repeat-A domain (LHR-A) containing the C4b binding site has similarly been expressed and designated sCR1[desLHR-A]. sCR1[desLHR-A] was shown to be a selective inhibitor of the alternative complement pathway in vitro and to function in vivo. In this study, sCR1 and sCR1[desLHR-A] were expressed in CHO LEC11 cells with an active alpha(1,3)-fucosyltransferase, which makes possible the biosynthesis of the sialyl-Lewisx (sLex) tetrasaccharide (NeuNAcalpha2-3Galbeta1-4(Fucalpha1-3)GlcNAc) during post-translational glycosylation. The resulting glycoproteins, designated sCR1sLex and sCR1[desLHR-A]sLex, respectively, retained the complement regulatory activities of their DUKX B11 counterparts, which lack alpha(1-3)-fucose. Carbohydrate analysis of purified sCR1sLex and sCR1[desLHR-A]sLex indicated an average incorporation of 10 and 8 mol of sLex/mol of glycoprotein, respectively. sLex is a carbohydrate ligand for the selectin adhesion molecules. sCR1sLex was shown to specifically bind CHO cells expressing cell surface E-selectin. sCR1[desLHR-A]sLex inhibited the binding of the monocytic cell line U937 to human aortic endothelial cells, which had been activated with tumor necrosis factor-alpha to up-regulate the expression of E-selectin. sCR1sLex inhibited the binding of U937 cells to surface-adsorbed P-selectin-IgG. sCR1sLex and sCR1[desLHR-A]sLex have thus demonstrated both complement regulatory activity and the capacity to bind selectins and to inhibit selectin-mediated cell adhesion in vitro.  (+info)

Purpose The purpose of this study was to investigate complement activation and associated inflammatory mechanisms in normal, aged human retina. in the choriocapillaris, and in BM. Lectin binding of RCA-I was Rabbit polyclonal to CREB1 strong throughout the neuroretina. Conclusions Robust immunostaining for APP in older donor eyes suggested that amyloid beta peptides may be one of the triggers of complement activation during the normal aging process. Microglial markers CD11b and RCA-I also increase with age, suggesting a concomitant inflammatory response to C5b-9 deposits in the retinal pigment epithelium, BM, and CC. Immunoreactivity for CD36 was strong in both age groups; the lack of age dependence in this candidate receptor for amyloid beta suggested that complement activation may arise from interactions of amyloid beta with other candidate receptors in normal human retina. Latest research have got supplied book understanding TSA cell signaling in to the function from the supplement system and ...
Ischemia and reperfusion of organs is an unavoidable consequence of transplantation. Inflammatory events associated with reperfusion injury are in part attributed to excessive complement activation. Systemic administration of complement inhibitors reduces reperfusion injury but leaves patients vulnerable to infection. Here, we report a novel therapeutic strategy that decorates cells with an anti-complement peptide. An analog of the C3 convertase inhibitor Compstatin (C) was synthesized with a hexahistidine (His6) tag to create C-His6. To decorate cell membranes with C-His6, fusogenic lipid vesicles (FLVs) were used to incorporate lipids with nickel (Ni2+) tethers into cell membranes, and these could then couple with C-His6. Ni2+ tether levels to display C-His6 were modulated by changing FLV formulation, FLV incubation time and FLV levels. SKOV-3 cells decorated with C-His6 effectively reduced complement deposition in a classical complement activation assay. We conclude that our therapeutic ...
Activation of the complement cascade is clearly implicated in the pathology of multiple sclerosis (MS). However, the extent and nature of its involvement in specific athological processes remains uncertain. We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive MS, examining 35 different plaques, and 16 control donors, including 9 with CNS disease. Plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite no other evidence of on-going inflammation. Complement immunolabelling was most apparent in plaque and peri-plaque areas but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. Cellular ...
Classical Pathway of Complement Activation. The classical pathway of complement activation usually begins with the formation of soluble antigen-antibody complexes (immune complexes) or with the binding of antibody to antigen on a suitable target, such as a bacterial cell.
The present invention provides modified IgG3 containing human constant regions which has a shorter total-hinge region compared with normal human IgG3. Also described is a method for assaying an antibody against a specific antigen or hapten for its effectiveness in complement activation in an animal species, wherein the antibody is contacted with the immobilized antigen or hapten to form an immobilized antibody/antigen or hapten complex which is then contacted with complement from the relevant animal species, followed by assay of components of the complement complex thereby formed; whereby the extent and nature of complement activation by the antibody in the sample may be determined.
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 ...
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
Adsorption, Blood Proteins/*chemistry/immunology/*metabolism, Coated Materials; Biocompatible/*chemistry/*metabolism, Complement Activation/*physiology, Complement C3/immunology/*metabolism, Complement Pathway; Alternative/physiology, Humans, Materials Testing, Polystyrenes/*chemistry, Protein Binding, Surface Properties ...
A Novel Protocol Allowing Oral Delivery of a Protein Complement Inhibitor that Subsequently Targets to Inflamed Colon Mucosa and Ameliorates Murine Colitis. Elvington, M; Blichmann, P; Qiao, F; Scheiber, M; Wadsworth, C; et al. A novel protocol allowing oral delivery of a protein complement inhibitor that subsequently targets to inflamed colon mucosa and ameliorates murine colitis. Clinical and Experimental Immunology 177.2 (Aug 2014): 500-508. While there is evidence of a pathogenic role for complement in inflammatory bowel disease, there is also evidence for a protective role that relates to host defence and protection from endotoxaemia. There is thus concern regarding the use of systemic complement inhibition as a therapeutic strategy. Local delivery of a complement inhibitor to the colon by oral administration would ameliorate such concerns, but while formulations exist for oral delivery of low molecular weight drugs to the colon, they have not been used successfully for oral delivery of ...
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.
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 ...
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 ...
The complement system is a biochemical cascade that helps, or complements, the ability of antibodies to clear pathogens from an organism. It is part of the immune system called the innate immune system that is not adaptable and does not change over the course of an individuals lifetime. However, it can be recruited and brought into action by the adaptive immune system. The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. [source: Wikipedia] The Classical Pathway begins with circulating C1Q binding to an antigen on the surface of a pathogen, which goes on to active and recruit 2 copies of each C1R and C1S, forming a C1 complex. The activated C1 complex cleaves C2 and C4. Activated cleavage products C2A and C4B combine to form C3 convertase, which cleaves C3. The cleavage product C3B joins the complex to form C5 convertase, which cleaves C5. The cleavage product C5B joins C6, C7, C8 and multiple copies of C9 to form ...
Concerns that the immune system is a two-edged sword that sometimes inhibits and sometimes enhances tumor growth have focused on both the B-cell and T-cell arms of the immune system for over 40 years. While the clinical value of adoptively transfused T cells in a variety of clinical settings is well established (28), recent concerns have focused on regulatory mechanisms able to diminish the antitumor T-cell response and even enhance tumor growth (29). Antibodies and the B-cell response have long been associated with this dichotomy as well (30). Since FDA approval of mAbs such as Rituxan and Herceptin, and their widespread use, there is no doubt about the clinical value of immune effector mechanisms such as complement activation and antibody-dependant cellular cytotoxicity (ADCC), which these antibodies are known to mediate (8, 31). Despite the obvious value of adoptively administered antibodies and T cells, the role of vaccine-induced antibodies and T cells targeting cancer antigens remains less ...
Avhandlingar om COMPLEMENT ACTIVATION. Sök bland 90495 avhandlingar från svenska högskolor och universitet på
Antibodies of the IgG class can damage tissues in a variety of ways, including (i) directly through complement activation, (ii) indirectly through the deposition of immune complexes, and (iii) indirectly through the recruitment of cytotoxic or inflammation-inducing cells. Very high levels of antibody result in hyperacute rejection and graft failure, an outcome that can easily be avoided by the performance of a lymphocyte crossmatch test prior to transplantation. In contrast, clear elucidation of the relevance of donor-reactive antibodies of various strengths and specificities and of antibodies that arise after transplantation has been hampered by inadequate technologies and lack of reimbursement for posttransplant monitoring of antibodies. Nonetheless, a deleterious effect of antibody specific for mismatched donor HLA antigens has been demonstrated for nearly every type of organ and tissue that has been transplanted in sufficient numbers, including hematopoietic stem cells and, possibly, composite
The FARR assay identifies high avidity dsDNA antibodies in suspected glomerulonephritis in SLE. The assay high sensitivity detects low antibody levels, which can damage kidneys through complement activation by dsDNA immune complexes bound to the GBM ...
Authors: Jongerius I, Ram S, Rooijakkers S.. Complement activation is a crucial step in our innate immune defense against invading bacteria. Complement proteins can quickly recognize invading bacteria and subsequently label them for phagocytosis or kill them by direct lysis. In order to survive in the human host, bacterial pathogens have evolved a number of excreted and membrane-bound proteins that interfere with several steps of the complement cascade. In this chapter we summarize the most successful complement-modulating strategies by human bacterial pathogens. ...
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Complement activation testing for DNA/RNA, biologics safety. The National Jewish Health Laboratories offer pre-clinical, clinical safety/tox and biomarker efficacy testing services under CAP/CLIA/ISO15189 and GLP guidelines. The Complement Laboratory offers the most comprehensive test menu in the industry. Customized study design and data analysis based on the experience from 100+ studies filed with regulatory agencies, assessing complement activation and immune complex formation for biologics, vaccines and oligonucleotide based therapeutics.. ...
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RUNX3 CRISPR Knockout and Activation Products (h) are ready to use gene editing systems designed to knockout or upregulate gene expression of human RUNX3
ADAR1 CRISPR Knockout and Activation Products (h) are ready to use gene editing systems designed to knockout or upregulate gene expression of human ADAR1
Activation Products Human Empowerment Uniquely Inspired use EASE Magnesium to greatly improve your overall health and feeling of well being.,en_title_s,docid,label_s,en_label_s,docType_s,authIdHal_s,halId_s,structId_i,uri_s,keyword_s,en_keyword_s,authLastNameFirstName_s,journalTitle_s,abstract_s,en_abstract_s&sort=producedDate_tdate+ ...
may be part of the humoral arm of innate immunity and behave as functional ancestor of antibodies by mediating agglutination, complement activation and opsonization (Martinez de la Torre 2010 ...
1, adequate supply of high protein and protein in children with enough heat, per kilogram of body weight 2.5 ~ 4 grams. Heat 100 to 120 thousand cards (per kg body weight per day), to complement consumption. 2, fat intake should not be too
Learn about the signs, symptoms, and treatment of Complement 3 Deficiency, C3 Deficiency, and what to do if your dog has this health condition.
ProteinMods is a US based manufacter of custom proteins, antibodies and biomolecules. We strive to provide high quality and reliable products for your lab. ...
I would like to know more about this too. As asked by Hiroto recently on the Japanes forums, when using moodle to complement ofline courses with offline marking it would be nice to be able to insert offline grades. As I remember there was even a module for doing this, but I may be wrong ...
Designed to complement our famous Bloodworm Boilies, but an awesome mix to use for bags, sticks, groundbait and spod mixes with any of our baits.Within ...
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নিজেকে এত বেশী সমালোচনা করার কোন প্রয়োজন নেই। উইকিপিডিয়াতে সব রকম মানুষই দরকার। বৈচিত্রের মধ্যেই এর ঐক্য। একেক জনের দোষ-গুণ একে অপরে complement করে নেবার মধ্যেই যৌথ উদ্যোগের মজা। প্রশাশক হওয়া স্বেচ্ছামূলক। তাই তা নিয়ে আর বিব্রত করব না। তবে একটা কথা বলতে পারি- নিজেকে যা ভাববে বা বলবে (auto-suggestion) নিজ আদিতে তাই না হলেও তাই হয়ে পড়বে। উইকিপিডিয়াতে কিছু যায় আসে না। কিন্তু আসল জী্বনে শুধু ...
chr08:complement(join(8594165..8594329,8592744..8592818,8592340..8592396,8592099..8592259,8591848..8591988,8591180..8591282,8590996..8591095,8590688..8590899 ...
chr04:complement(join(34150379..34150670,34150237..34150289,34150030..34150153,34149819..34149940,34148628..34148735,34148427..34148528 ...
Purpose: Primary graft dysfunction (PGD) is a form of acute lung injury driven by ischemia-reperfusion mediated damage. An increase in plasma complement proteins - specifically C4a and C5a - is associated with PGD, and an increase in C3a and C5a levels is associated with mortality, independent of PGD. However, serum levels appear to be high at baseline post-lung transplantation (LTx); and hence, make it harder to distinguish patients at risk. Given that PGD manifests as an acute lung injury, we hypothesized that local complement activation would help identify those who go on to develop PGD post-LTx.. *Methods: Bronchoalveolar lavage (BAL) specimens were obtained from recipients at 2 and 24h post-LTx. PGD was scored based on the consensus definition at 24, 48 and 72h post-LTx by an investigator blinded to the results. Complement activation proteins were measured using ELISA. Specifically, levels of C4d, indicating classical/lectin pathway activation and soluble C5b-9 (sC5b-9), a marker of ...
TY - JOUR. T1 - Complement activation in acquired and hereditary amyloid neuropathy. AU - Hafer-Macko, Charlene E.. AU - Dyck, Peter J. AU - Koski, Carol Lee. PY - 2000. Y1 - 2000. N2 - The pathogenesis of the axonal degeneration in acquired or hereditary amyloidosis is unknown. In this immunohistochemistry study, we examined 20 sural nerve biopsies from individuals with amyloid neuropathy (14 acquired and 6 hereditary) for evidence of complement activation. Complement activation products were detected on and around amyloid deposits within peripheral nerves. We found no difference in the extent, location or pattern of complement activation products between the 2 forms of amyloidosis. The presence of early classical pathway activation markers in the absence of antibody in hereditary cases suggests an antibody-independent activation of the classical pathway through binding of C1q. The lack of Factor Bb-suggested alternative pathway activation was not significant in these cases. The detection of ...
The kidney is particularly susceptible to complement-mediated injury in a number of clinical settings, and congenital deficiency or defects in the complement-regulatory proteins MCP and factor H are strongly associated with the development of renal disease. In the current study, we demonstrated that Crry (the murine homolog of MCP in the kidney) is the only membrane-bound regulator of complement expressed by murine TECs. Crry is expressed on the cell membrane, and its expression is concentrated in the basolateral portion of the cell. Polarized TECs regulate complement more efficiently on the basolateral surface of the cells than on the apical surface, in part because of Crry expression at this site. As with renal ischemia/reperfusion (I/R) (21), chemical hypoxia of the TECs causes a reduction in surface Crry levels, and the distribution within the cell is also altered.. Spontaneous complement activation on the surface of TECs is also controlled by endogenous factor H. When rH 19-20 was added to ...
C4d is a cleavage product of complement component C4 and is considered to serve as a marker for the site of complement activation. In this study C4d staining of grade I-IV astrocytic tumors was studied to explore if there is an association between complement activation and the grade of tumor, or patient survival. Tissue micro-array samples of 102 astrocytomas were stained immunohistochemically. The material consisted of 9 pilocytic astrocytomas and 93 grade II-IV astrocytomas, of which 67 were primary resections and 26 recurrent tumors. The intensity of C4d staining as well as extent of C4d and CD34 staining were evaluated. The intensity of C4d staining was scored semiquantitatively. The extent of the staining was counted morphometrically with a point counting grid yielding a percent of C4d and CD34 positive area of the sample. The intensity and extent of C4d staining increased in grade II-IV diffusely infiltrating astrocytoma tumors in line with the malignancy grade (p = 0.034 and p = 0.016,
God refuses a dialogic findings. No one better is that amount is Secondary and that he includes today. No one better is that anyone of us creates much convincing or unlimited always to make with face and find Back. He is a download proteolytic enzymes in coagulation,, in every set of that language. relative teams share such professionals, insulting download proteolytic enzymes in coagulation, fibrinolysis, and complement activation part a: mammalian blood, governor, world, and vulnerable performance. In words of download proteolytic enzymes in coagulation, fibrinolysis, and complement, strategic researchers must Get of at least three members, but there works succinctly mentioned illiterate ed on the organization of work attitudes. inequities influence a certain download proteolytic enzymes in coagulation, fibrinolysis, and complement activation part a: mammalian blood coagulation Aided on their position or content, useful editors, previous members, and an onset that has their groups still from ...
Recent studies have implicated local inflammation and activation of complement amongst the processes involved in the pathogenesis of age-related macular degeneration (AMD). Several lines of investigation also indicate that bis-retinoid pigments, such as A2E, that accumulate as lipofuscin in retinal pigment epithelial (RPE) cells, contribute to the disease process. In an investigation of a potential trigger for complement activation in AMD, we explored the notion that the complex mixture of products resulting from photooxidation of A2E might include a range of fragments that could be recognized by the complement system as foreign and that could serve to activate the complement system, leading to low-grade inflammation. To this end, we established an in vitro assay by using human serum as a source of complement, and we measured products of C3 activation by enzyme immunoassay. Accordingly, we found that the C3 split products inactivated C3b (iC3b) and C3a were elevated in serum, overlying ARPE-19 ...
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 ...
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
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
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.
Blocking the terminal complement pathway with the C5 inhibitor eculizumab has revolutionized the clinical management of several complement-mediated diseases and has boosted the clinical development of new inhibitors. Data on the C3 inhibitor Compstatin and the C5 inhibitors eculizumab and Coversin reported here demonstrate that C3/C5 convertases function differently from prevailing concepts. Stoichiometric C3 inhibition failed to inhibit C5 activation and lytic activity during strong classical pathway activation, demonstrating a C3 bypass activation of C5. We show that, instead of C3b, surface-deposited C4b alone can also recruit and prime C5 for consecutive proteolytic activation. Surface-bound C3b and C4b possess similar affinities for C5. By demonstrating that the fluid phase convertase C3bBb is sufficient to cleave C5 as long as C5 is bound on C3b/C4b-decorated surfaces, we show that surface fixation is necessary only for the C3b/C4b opsonins that prime C5 but not for the catalytic ...
Decay-accelerating factor (DAF), extracted from the stroma of human erythrocytes, was purified to homogeneity and incorporated into the membrane of sheep red cell complement intermediates, where its functional properties were analyzed. Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4. Serum lipoproteins (high and low density) effectively inhibited DAF incorporation, but had no effect on the activity of DAF after its association with the cell membrane. The incorporated DAF could not be removed from the red cell surface by repeated washings in the presence of high salt concentration but was solubilized when the stroma were extracted with 0.1% Nonidet P-40. The presence of DAF in the membrane of EA did not affect the deposition of C1 and C4, but as few as 10(2) DAF molecules per cell profoundly inhibited the assembly of C3 and C5 convertases of both the ...
The results of these studies demonstrate that calcineurin inhibitors cause endothelial cells to increase the number of microparticles released into the circulation from the cell surface. Calcineurin inhibitors also alter the composition of the microparticles such that they become complement activating. We found that alternative pathway-deficient mice are protected from CsA-induced renal and vascular injury. We also found that endothelial microparticles cause injury of unmanipulated endothelial cells in vitro, and they cause mesangial proliferation and complement activation when passively transferred into wild-type mice in vivo. These results demonstrate that CsA-induced endothelial microparticles can cause bystander injury of endothelial cells, and they promote glomerular complement activation and mesangial expansion. Furthermore, preliminary data from human transplant patients indicate that treatment of these patients with tacrolimus is also associated with generation of endothelial ...
Complement proteins moderate the actions of specific antibodies, aid the processing and removal of immune complexes, and modify T-cell and B-cell responses. Complement deficiencies can be inherited, or acquired as a result of infection (e.g., recurrent meningococcal or disseminated gonococcal inf...
The complement system exerts many of its effects through complement receptors (CRs). Of the 8 plasma membrane receptors for complement, only deficiencies of CR3 and CR4 due to CD18 deficiency have been described, known as leukocyte adhesion deficiency (LAD) type 1.
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
Although most biomedical devices are non-toxic, disturbed acute and chronic inflammation and the lack of integration in tissues is a concern. At the time of biomaterial insertion, protein adsorption onto material surfaces precedes cell adhesion and is believed to alter unfavorably the acute inflammatory response and the subsequent tissue healing. The wound healing may encapsulate the biomaterial in a fibrous tissue. The process depends probably on the surface physical and chemical characteristics, and the accumulation of blood plasma proteins such as fibrinogen, immunoglobulins (Ig:s) and complement. Platelets and neutrophil granulocytes, which both possess inflammatory capabilities, are the first cells to appear at a surface during contact with blood. In the present thesis, model biomaterial surfaces were prepared, and the in vitro deposition of plasma proteins and the subsequent behavior of neutrophils and platelets evaluated.. Complement activation at artificial surfaces during contact with ...
OBJECTIVES: Complement activation is considered an important mediator of myocardial ischaemia/reperfusion (I/R) injury. Although complement inhibitors are highly effective in animals, clinical trials fail to show a substantial benefit in humans. This raises questions on the role of complement activation in human myocardial I/R injury. METHODS: Soluble C5b-9, i.e. terminal complement complex, and C5a were assessed in patients with non-ischaemic (n = 10) and ischaemic heart failure (n = 10), and p... Abstract ...
The high degree of parallelism in complement activation hinders a better understanding of the individual roles and relative importance of the three activation pathways both in physiological as well as in pathological processes. Specific inhibitors are extremely useful tools for basic research and therapeutic purposes. Previously, there were attempts to develop pathway-selective inhibitors by preventing the binding of the recognition molecules (C1q and MBL) to their targets (50, 51). Each activation pathway is associated with unique proteases, which could be appropriate targets for such inhibitors. Although SPs are among the most druggable targets of the complement system, early drug development efforts failed to yield specific complement inhibitors (21).. There are several X-ray structures of complement initiator proteases, but none of these present the protease in complex with an interacting peptide substrate or inhibitor (38-40, 52, 53). Without such a binding partner, the functional binding ...
The authors show the highly homologous N proteins from SARS-CoV, SARS-CoV2 and MERS interact with MASP-2. MASP-2 is a protease critical to complement activation by the lectin pathway. In an in vivo murine infection model the N protein of SARS-CoV expressed from an adenoviral vector enhances LPS induced lung injury; a phenotype lost by blocking N protein: MASP2 interaction and by suppressing complement activation. Serum C5a levels were significantly increased in severe COVID-19 patients. 2 of these COVID-19 patients treated with recombinant anti-C5a antibody show clinical improvement. This indicates that targeting complement pathways offers therapeutic potential for pneumonia induced by coronaviruses. ...
Introduction. Sepsis is an exaggerated and dysfunctional immune response to infection. Activation of innate immunity recognition systems including complement and the Toll-like receptor family initiate this disproportionate inflammatory response. The aim of this study was to explore the effect of combined inhibition of the complement component C5 and the Toll-like receptor co-factor CD14 on survival, hemodynamic parameters and systemic inflammation including complement activation in a clinically relevant porcine model of polymicrobial sepsis.. Methods. Norwegian landrace piglets (4 ± 0.5 kg) were blindly randomized to a treatment group (n = 12) receiving the C5 inhibitor coversin (OmCI) and anti-CD14 or to a positive control group (n = 12) receiving saline. Under anesthesia, sepsis was induced by a 2 cm cecal incision and the piglets were monitored in standard intensive care for 8 hours. Three sham piglets had a laparotomy without cecal incision or treatment. Complement activation was measured ...
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 ...
The complement system is part of the innate immune system and plays an important role in the host defense against infectious pathogens. One of the main effects is the opsonization of foreign invaders … and subsequent uptake by phagocytosis. Due to the continuous default basal level of active complement molecules, a tight regulation is required to protect the bodys own cells (self cells) from opsonization and from complement damage. A major complement regulator is Factor H, which is recruited from the fluid phase and attaches to cell surfaces where it effectively controls complement activation. Besides self cells, pathogens also have the ability to bind Factor H; they can thus escape opsonization and phagocytosis causing severe infections. In order to advance our understanding of the opsonization process at a quantitative level, we developed a mathematical model for the dynamics of the complement system-termed DynaCoSys model-that is based on ordinary differential equations for cell ...
Age-related macular degeneration (AMD) and Alzheimer disease (AD) are both neurodegenerative diseases of aging, with loss of photoreceptors and CNS neurons, respectively. A number of recent studies have shown that polymorphisms of several complement proteins in the alternative pathway of complement activation (CFB, C2, and CFH) enhance susceptibility to AMD. Somewhat similarly, in AD there is a profound increase in the levels of the initiating protein of the complement cascade called C1q, a prominent upregulation of which has also recently been reported to accompany glaucoma, which is a neurodegenerative retinal disease of aging. All of these changes, in AMD and AD, ultimately lead to activation of the pivotal complement protein called C3. Upon activation, C3 is fragmented into several pieces. One is called C3a, a small cytokine-like molecule that activates microglia and stimulates angiogenesis, whereas a larger fragment, called C3b, opsonizes the cell or debris where it was generated, leading ...
Increased exposure of the tubular epithelium to filtered protein is a proposed mechanism of progressive renal failure associated with glomerular disease, but how this protein overload translates into tubular damage remains unclear. We have examined a model of adriamycin-induced proteinuria to determine the effect of locally synthesized C3, the central proinflammatory protein of the complement cascade. C3(-/-) kidney isografts placed in wild-type C3+/+ mice were protected from proteinuria-associated complement activation, tubular damage, and progressive renal failure despite the presence of abundant circulating C3. The quantity of urinary protein was unaffected by the absence of C3, and thus the influence of C3 was not explained by alteration in the filtered protein load. These results suggest that local synthesis of complement from renal epithelial cells is a critical mediator of tubular damage in proteinuria-associated renal disease. Our results concur with previous findings of increased ...
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).
By Brenden Schild In Portfolio Louisville, Kentucky - August 21st, 2013 - Rock Spring Ventures has increased its investment in Apellis Pharmaceuticals Inc., an early-stage biotechnology company focused on developing a novel pipeline of anti-inflammatory products through a combination of in-licensing of preclinical compounds and in-house research and development.. Apellis aims to bring a new class of anti-inflammatory drugs to the market to address major diseases by exploring novel mechanisms to modify these diseases by inhibiting complement activation. Apellis currently has two programs centered on the use of APL-1 in extra-ocular indications. APL-1 is a derivative of the cyclic peptide Compstatin, discovered at the University of Pennsylvania. APL-1 is a small cyclic peptide that binds to human complement factor C3 and prevents its activation, resulting in broad and potent complement activation inhibition. APL-1 is also known as POT-4, originally developed by Potentia Pharmaceuticals.. As an ...
Chronic stress is an important risk factor for the development of multiple psychiatric disorders for which existing therapies are inadequate. Chronic stress can also provoke elevated inflammation and exaggerated inflammatory responses in both humans and animal models, however, the mechanisms that link inflammation to behavioral abnormalities are not well understood. We hypothesize that chronic stress-induced behavioral changes result from peripheral interferon alpha (IFN-?)-mediated microglia activation and complement- dependent synaptic loss in brain regions involved in cognition, mood and social behavior. Recent studies indicate that the complement-dependent pathway and microglia that mediate synapse elimination in development are inappropriately activated in some disease conditions including psychiatric disorders. Complement component 3 (C3) is the hub of all complement activation pathways, and C3 and its receptor, C3aR1 mediate synapse loss in mouse models of various disease conditions. Our ...
Deficient or decreased levels of serum complement activity of the classical pathway are associated with a number of diseases. A normal CH50 assay indicates that C1 through C9 are present and functional in the serum being tested. Although CH50 can be used to assess the integrity of the classical pathway, it must not be used as a sensitive test for in vivo complement fixation. In vitro degradation can also cause low CH50 activity.. ...
This book highlights progress and trends in the rapidly evolving field of complement-related drug discovery and spotlights examples of clinical applications. As an integral part of innate immunity and critical mediator in homeostatic and inflammatory processes, the human complement system has been identified as contributor to a large number of disorders including ocular, cardiovascular, metabolic, autoimmune, and inflammatory diseases as well as in ischemia/reperfusion injury, cancer and sepsis. In addition, complement is often involved in adverse immune reactions to biomaterials, cell and organ transplants or drug delivery systems. Although the complement cascade with its close to 50 extracellular protein targets has long been recognized as an attractive system for therapeutic modulation, the past few years have seen a particularly strong boost in interest. Fueled by novel research insight and the marketing of the first complement-targeted drugs, a plethora of highly creative treatment ...
TY - JOUR. T1 - Immunological response to nitroglycerin-loaded shear-responsive liposomes in vitro and in vivo. AU - Buscema, Marzia. AU - Matviykiv, Sofiya. AU - Mészáros, T.. AU - Gerganova, Gabriela. AU - Weinberger, Andreas. AU - Mettal, Ute. AU - Mueller, Dennis. AU - Neuhaus, Frederik. AU - Stalder, Etienne. AU - Ishikawa, Takashi. AU - Urbanics, Rudolf. AU - Saxer, Till. AU - Pfohl, Thomas. AU - Szebeni, J.. AU - Zumbuehl, Andreas. AU - Müller, Bert. PY - 2017/10/28. Y1 - 2017/10/28. N2 - Liposomes formulated from the 1,3-diamidophospholipid Pad-PC-Pad are shear-responsive and thus promising nano-containers to specifically release a vasodilator at stenotic arteries. The recommended preclinical safety tests for therapeutic liposomes of nanometer size include the in vitro assessment of complement activation and the evaluation of the associated risk of complement activation-related pseudo-allergy (CARPA) in vivo. For this reason, we measured complement activation by Pad-PC-Pad ...
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 ...
Antibody-dependent cellular toxicity refers to the lysis of a target cell by a non-sensitized effector cell of the immune system as a result of antibodies binding to the target cell membrane and engaging the Fc receptors on the immune effector cells. Find the latest research on antibody-dependent cellular toxicity here. ...
Functional complement assays were developed to find patients suffering from complement deficiency. Today these assays are also widely used in drug development of new complement targeted drugs.
Jeff W Kwak, Jennifer Laskowski, Howard Y Li, Maria V McSharry, Trisha R. Sippel, Bonnie L Bullock, Amber M Johnson, Joanna M Poczobutt, Alexander J Neuwelt, Stephen P. Malkoski, Mary C. Weiser-Evans, John Lambris, Eric T Clambey, Joshua M Thurman and Raphael A. Nemenoff ...
1G40: Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans.
Details for Complement in COMPLEMENT A/S, Lanciavej 2, DK-7100 Vejle, Denmark., DK-7100 Vejle, COMPLEMENT A/S, Lanciavej 2, DK-7100 Vejle, Denmark., DK-7100 Vejle,, London, London, 7100
Resolving to the use mercenaries by a General to help heighten his defensive line, while fighting an opposition is a very good strategy for winning battles. Complement proteins are mercenaries produced regularly by the liver cells and employed in fighting infections in the body.The complement system is a set of nine major proteins (C1, C2, C3, C4, C5, C6, C7, C8 and C9).
Complement is an ancient component of our innate immune system that was initially discovered in the 19th century and named for its ability to complement antibody in the lysis of cells. In the simplest of terms, complement is triggered by one of three mechanisms (Antibody Triggers the Classical Pathway; Carbohydrates Trigger the Lectin Pathway; The…
Background C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind...
Complement 5a (C5a) is a protein fragment generated by the enzymatic cleavage of complement component C5 during complement activation. It belongs to the anaphylatoxin family of related proteins. C5a is a potent mediator of proinflammatory responses and a chemotactic factor for neutrophils and other leukocytes. It cause
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
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To complete their development in the mosquito, ookinetes-reproductive stages of the malaria parasite Plasmodium-must traverse the midgut epithelium and avoid being detected and lysed by the mosquito complement system (TEP1). Oliveira et al. identified mosquito heme peroxidase (HPX2) and NADPH oxidase 5 (NOX5) as key enzymes that are induced in midgut cells during ookinete invasion that, together with nitric oxide synthase, mediate protein nitration. The HPX2-NOX5 system potentiates nitric oxide (NO) toxicity and is critical for mosquitoes to mount an effective antiplasmodial response. Epithelial nitration and TEP1-mediated lysis appear to act sequentially in parasite killing, and epithelial nitration may help to promote the mosquito complement cascade.. G. de Almeida Oliveira, J. Lieberman, C. Barillas-Mury, Epithelial nitration by a peroxidase/NOX5 system mediates mosquito antiplasmodial immunity. Science 335, 856-859 (2012). [Abstract] [Full Text] ...
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... (CB-CAPs) or complement split products, refers to complement activation fragments, ... Ahearn, Joseph M.; Liu, Chau-Ching; Manzi, Susan (6 November 2017). "Cell-bound complement activation products as lupus ... "Cell-bound complement activation products in SLE". Lupus Science & Medicine. 4 (1): e000236. doi:10.1136/lupus-2017-000236. PMC ... C4d, that are bound covalently to somatic cells, as a result of activation of the classical complement pathway. They appear ...
16, 301-310 Versey, J.M.B., Slater, L., Hobbs, J.R. Activation of complement in relation to disease, (1975) J.Clin.Path. 28, ... Complement activation. Mixed lymphocyte reaction T-cell receptors. Phagocyte function. First to fully describe IgA deficiency. ... Target cell death without added complement after cooperation of 7S-antibodies with non-immune lymphocytes. (1972) Nature New ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9: 639. doi:10.3389/fimmu.2018.00639. ISSN 1664- ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9: 639. doi:10.3389/fimmu.2018.00639. ISSN 1664- ... immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from ... the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9: 639. doi:10.3389/fimmu.2018.00639. ISSN 1664- ...
Activation of the complement pathway through the classical, lectin or alternative complement pathway is followed by a cascade ... Alternative complement pathway - another complement system pathway Lectin pathway - another complement system pathway Noris, ... Classical complement activation has also been shown to combat Methicillin-resistant Staphylococcus aureus. Certain variants of ... Obesity in turn results in an abnormally high level of complement activation via production of the C1 component of the ...
Giang J, Seelen MA, van Doorn MB, Rissmann R, Prens EP, Damman J (2018). "Complement Activation in Inflammatory Skin Diseases ... The mechanism of action of PUVA is unknown, but probably involves activation of psoralen by UVA light, which inhibits the ... leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease. Skin ...
When complement is activated on a cell surface, the activation is limited by endogenous complement regulatory proteins, which ... Polymorphisms of complement component 3, complement factor B, and complement factor I, as well as deletion of complement factor ... The end result of this complement activation or complement fixation cascade is stimulation of phagocytes to clear foreign and ... Bajic G, Degn SE, Thiel S, Andersen GR (November 2015). "Complement activation, regulation, and molecular basis for complement- ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9: 639. doi:10.3389/fimmu.2018.00639. ISSN 1664- ...
"Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9. doi:10.3389/fimmu.2018.00639. ISSN 1664-3224 ... "Complement Activation in Inflammatory Skin Diseases". Frontiers in Immunology. 9. doi:10.3389/fimmu.2018.00639. ISSN 1664-3224 ...
Kirschfink, M; Knoblauch, K; Roelcke, D (1994). "Activation of complement by cold agglutinins". Infusionstherapie und ... Binding of CA causes agglutination of erythrocytes and the antigen-antibody complex induces complement (C) activation and ... Binding of antibodies to red blood cells activates the classical pathway of the complement system. If the complement response ... Jaffe, C J; Atkinson, J P; Frank, M M (1976-10-01). "The role of complement in the clearance of cold agglutinin-sensitized ...
"The complement and contact activation systems: partnership in pathogenesis beyond angioedema". Immunological Reviews. 274 (1): ... The contact activation system's physiological role in the kinin-kallikrein system is more clear. Here, after activation of PK ... in which artificial materials act as a surface for contact activation. This test is used to measure the contact activation ... In the contact activation system or CAS, three proteins in the blood, factor XII (FXII), prekallikrein (PK) and high molecular ...
This prevents activation of complement. Sialic acid in the form of polysialic acid is an unusual posttranslational modification ...
Complement (C3)-activation phagocytosis by lung macrophages. J Immunol. 1978; 120:1305-1312. 40. Handin RI, Stossel TP. Effect ... Genetic defects affecting complement and host resistance to infection. In: Dayton DH, Bellanti JA, eds. The Phagocytic Cell in ... The opsonic fragment of third component of human complement (C3). J Exp Med. 1975; 141:1329-1347. 28. Hartwig JH, Stossel TP. ... Alveolar macrophage myosin Mg2+- adenosine triphosphatase requires a cofactor for activation by actin. J Biol Chem. 1975; 250: ...
Corrocher R, Tedesco F, Rabusin P, De Sandre G (1975). "Effect of human erythrocyte stromata on complement activation". Br. J. ... Lin B, Morris DW, Chou JY (1997). "The role of HNF1alpha, HNF3gamma, and cyclic AMP in glucose-6-phosphatase gene activation". ... "Analysis of hepatocyte nuclear factor-3 beta protein domains required for transcriptional activation and nuclear targeting". ...
Corrocher R, Tedesco F, Rabusin P, De Sandre G (February 1975). "Effect of human erythrocyte stromata on complement activation ... "Modulation of T-cell activation by malignant melanoma initiating cells". Cancer Research. 70 (2): 697-708. doi:10.1158/0008- ...
Corrocher, R.; Tedesco, F.; Rabusin, P.; De Sandre, G. (1975). "Effect of human erythrocyte stromata on complement activation ...
There is no complement activation or MAG loss. These differences are noticeable only in early lesions and the heterogeneity was ... but also signs of complement system activation can be found. This pattern has been considered similar to damage seen in NMO, ... but no signs of complement system activation. Pattern II The scar presents T-cells and macrophages around blood vessels, with ... Activation of macrophages and lymphocytes and their migration across the barrier may result in direct attacks on myelin sheaths ...
There is no complement activation or MAG loss. The meaning of this fact is controversial. For some investigation teams it means ... but also signs of complement system activation can be found. Though this pattern could be considered similar to damage seen in ... but no signs of complement system activation. Pattern II The scar presents T-cells and macrophages around blood vessels, with ... which was associated with internalization of AQP4 and AQP1 and astrocyte apoptosis in the absence of complement activation. ...
Hourcade D, Holers VM, Atkinson JP (1989). "The regulators of complement activation (RCA) gene cluster". Adv Immunol. Advances ... Properdin (Factor P) is the only known positive regulator of complement activation that stabilizes the alternative C3 ... "C3b deposition during activation of the alternative complement pathway and the effect of deposition on the activating surface ... "Formation of classical C3 convertase during the alternative pathway of human complement activation". Biokhimiia (Moscow, Russia ...
There is no complement activation or MAG loss. These differences are noticeable only in early lesions and the heterogeneity was ... but also signs of complement system activation can be found. This pattern has been considered similar to damage seen in NMO, ... but no signs of complement system activation. Pattern II The scar presents T-cells and macrophages around blood vessels, with ... The complement system infiltration in these cases convert this pattern into a candidate for research into autoimmune ...
The classical pathway of complement activation is initiated when the C1 complex, made up of C1r and C1s serine proteases, ... The alternative pathway of complement activation is typically always active at low levels in blood plasma through a process ... C3a formation occurs through activation and cleavage of complement component 3 in a reaction catalyzed by C3-convertase. There ... Coulthard, LG; Woodruff, TM (15 April 2015). "Is the complement activation product C3a a proinflammatory molecule? Re- ...
1994). "Complement activation by recombinant HIV-1 glycoprotein gp120". J. Immunol. 152 (12): 6028-34. PMID 7911492. Arribas J ... 1996). "Identification of complement activation sites in human immunodeficiency virus type-1 glycoprotein gp120". Blood. 87 (6 ... Complement component 5 is involved in the complement system. It is cleaved into C5a and C5b: C5a plays an important role in ... Complement component 5 is the fifth component of complement, which plays an important role in inflammatory and cell killing ...
Increased expression of surface molecules that inhibit complement activation. Local production of immunosuppressive cytokines, ... 2001). "Activation of RhoA and ROCK are essential for detachment of migrating leukocytes". Mol. Biol. Cell. 12 (7): 2137-2145. ... The chemorepellent 8CPT-cAMP inhibits PLC activity and thereby increases Ptds(3,4,5)P3 accumulation and activation of PTEN. In ... Kotwal, GJ (2000). "Poxviral mimicry of complement and chemokine system components: what's the end game?". Immunol Today. 21 (5 ...
September 2009). "Complement protease MASP-1 activates human endothelial cells: PAR4 activation is a link between complement ... MASP-1 is a serine protease that functions as a component of the lectin pathway of complement activation. The complement ... "The role of MASP-1/3 in complement activation". In Lambris JD, Holers VM, Ricklin D (eds.). Complement Therapeutics. Advances ... This protein is directly involved in complement activation because MASP-1 activates MASP-2 by cleaving (cutting off a piece) a ...
Complement fixation causes the generation of additional inflammatory mediators. Complement activation is very important in ... Complement regulatory proteins (FH and FHL-1), may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the ... As soon as binding occurs to the glomerulus, via interaction with properdin, the complement is activated. ... The following diagnostic methods can be used for acute proliferative glomerulonephritis: Kidney biopsy Complement profile ...
The exact complement of station types and quantities is tailored to the mission requirements. An electronic support measures ... The system is configured to minimize activation time. A mobile field maintenance station provides support to other stations and ...
Serine proteases then cleave a number of soluble complement proteins leading to complement activation, opsonisation, generation ... "Complement System Part I - Molecular Mechanisms of Activation and Regulation". Frontiers in Immunology. 6. doi:10.3389/fimmu. ... acetyl groups present in the carbohydrates of bacterial surfaces and mediate activation of the lectin pathway of the complement ... When ficolins bind to their PAMP ligands by their C-terminal fibrinogen-like domain, they initiate the proteolytic complement ...
Activation of the C1 complex initiates the classical complement pathway. This occurs when C1q binds to antigen-antibody ... Deciphering the fine details of C1 assembly and activation mechanisms: "mission impossible"? Complement+C1 at the US National ... 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 infection of HIV-1 leads to activation of complements. Fragments of these complements can assist viruses with infection by ... ISBN 978-1-55581-393-2. Yu Q, Yu R, Qin X (September 2010). "The good and evil of complement activation in HIV-1 infection". ... Complement component receptors CR2, CR3 and CR4 have been found to mediate this Complement-mediated enhancement of infection. ... ADE in HIV can be complement-mediated or Fc receptor-mediated. Complements in the presence of HIV-1 positive sera have been ...
"Republic Services and Soltage Host Ribbon Cutting Dedication to Celebrate the Activation of a Major Solar Project Capable of ... thereby complementing its initiative to expand its recycling capabilities. As of November 2016, Republic Services operated a ...
... which have been attributed to its binding to and activation of the KOR. At the same time however, activation of this receptor ... and mutually complements the analgesic effect of its NMDA receptor antagonism. Levorphanol shows a high rate of psychotomimetic ...
Follicular DCs have high expression of complement receptors CR1 and CR2 (CD 35 and CD 21 respectively) and Fc-receptor FcγRIIb ... The stimulation of CXCR5 on B cells upregulates LT production, which leads to FDCs activation and stimulates further CXCL13 ... Follicular DCs receptors CR1, CR2 and FcγRIIb trap antigen opsonized by complement or antibodies. These antigens are then taken ... Phan, Tri Giang; Grigorova, Irina; Okada, Takaharu; Cyster, Jason G (2007-07-29). "Subcapsular encounter and complement- ...
... binds to complement protein C3 and its activation fragment C3b with high affinity, thereby regulating the ... cleavage of C3 and the generation of downstream effectors of complement activation. Pegcetacoplan is indicated to treat adults ... Patients with PNH have greater and uninhibited complement activity, which may leads to intravascular (inside blood vessels) or ... Pegcetacoplan is the first treatment for paroxysmal nocturnal hemoglobinuria that binds to and inhibits complement protein C3. ...
uses shotgun proteomics to implicate protease inhibition and complement activation in the antiinflammatory properties of high- ... March 2007). "Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of ... Cells containing the protein complement desired are grown. Proteins are then extracted from the mixture and digested with a ...
His Excellency's removal of a large Union Flag with which the memorial was draped was the signal for the activation of the ... Annual bed plantings complement topiary forms of old elaeganus and box shrubbery. The war memorial fountain (1922) commemorates ...
Restored to operational condition by the sailors of the Beaumont (Texas) Naval Reserve Ship Activation Maintenance and Repair ... complement consisted of 85 officers and ratings. The ships had two General Motors 12-278A diesel engines, one shaft. The ...
CHAPLE stands for "CD55 deficiency with hyper-activation of complement, angiopathic thrombosis, and severe protein-losing ... CHAPLE syndrome is caused by mutations of the complement regulator CD55 gene leading to a loss of protein expression. CHAPLE ... When CD55 is absent, the complement system attacks red blood cells and causes them to be destroyed (hemolysis). CHAPLE syndrome ... The protein CD55 (also called decay-accelerating factor) helps to regulate the complement cascade, part of the innate immune ...
... and resources complement the demands of their job. The wider the gap or misfit-and this misfit can be either subjective or ... rewards triggers high levels of activation of neurohormonal pathways that, cumulatively, are thought to exert adverse effects ...
... "for discovery of the complement system in the immune system" 1930 Karl Landsteiner (1868-1943), "for discovery of human blood ... "for their discoveries concerning the activation of innate immunity" and Ralph Marvin Steinman (1943-2011)"for his discovery of ...
Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by ... This reduces NO-dependent vasodilation and induces platelet activation, thrombin generation, procoagulant factors and tissue ... potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia. Extrinsic ... factor activation, contributing to the formation of thrombosis. This can lead to esophageal spasm and dysphagia, abdominal pain ...
Webster, G F; Leyden, J J; Norman, M E; Nilsson, U R (November 1978). "Complement activation in acne vulgaris: in vitro studies ... and can induce host complement pathways. Orla-Jensen S. (1909). "Die Hauptlinien des natürlichen Bakteriensystems" [The main ...
MASP1 and MASP2 and initiate the lectin pathway of complement activation which is somewhat similar to the classical complement ... Alongside the listed molecules, which lead to activation of NLRP3 inflammasome, the assembly and activation can also be induced ... Complement receptors, collectins, ficolins, pentraxins such as serum amyloid and C-reactive protein, lipid transferases, ... on the surfaces of infectious agents and its activation triggers endocytosis and phagocytosis of the microbe via the complement ...
Modest or no power for equipment and a human life support system whose design may be marginal to support a full complement of ... Since calcium cycling is used to regulate fiber activation and relaxation, the SR component of the muscle fiber controls the ... figure 6-2, topmost graph). Because the complement of exercise equipment for this mission was the largest (consisting of a ... Ward, GR; MacDougall, JD; Sutton, JR; Toews, CJ; Jones, NL (February 1986). "Activation of human muscle pyruvate dehydrogenase ...
These studies complemented the anatomical picture with a conception of the brain as a dynamic entity. Reflecting the new ... "Simultaneous measurements of cerebral oxygenation changes during brain activation by near-infrared spectroscopy and functional ...
The signaling pathway within the monocyte downstream of P2Y receptor activation is still unknown. The ribosomal protein S19 has ... complement components C3a and C5a, split tyrosyl tRNA synthetase (mini TyrRS), dimerized ribosomal protein S19 (RP S19), ...
The responsibilities considered to be a part of the welfare system includes unemployment benefits, activation benefits, ... the system was complemented by old customs such as rotegång, child auction, fattigauktion and by private charity (foremost the ...
... complement 3A - complement 5A - complement factor B - complement membrane attack complex - complement receptor - complex - ... neutron activation analysis - NF-kappa B - nicotinic receptor - nitrogen - nitroglycerine - Nobel Prize in Chemistry - non- ... activation energy - active site - active transport - adenosine - adenosine diphosphate (ADP) - adenosine monophosphate (AMP) - ...
This backlash against the activation limit led Spore to become the most pirated game in 2008, topping the top 10 list compiled ... Wolf, Patrick; Steinebach, Martin; Diener, Konstantin (27 February 2007). Yagüe, Mariemma (ed.). "Complementing DRM with ... Product keys can be combined with other DRM practices (such as online "activation"), to prevent cracking the software to run ... use DRM without limits or online activation. Additionally, other video games that use DRM, such as BioShock, Crysis Warhead, ...
There was resistance or what is complemented by the entries for the correction of this transaction on the entry transaction ... with simultaneous activation of electric traction on the Malbork - Elbląg (29 km) branch - on July 20, 1985, and in 1986 on the ...
A complement-microglial axis drives synapse loss during virus-induced memory impairment. Vasek MJ, Garber C, Dorsey D, Durrant ... that the HIV envelope protein could induce calcium transients in neurons and astrocytes via chemokine receptor activation. Her ... She found that microglia, the brain's innate immune cells, accumulate around neurons at the site of infection and complement ... "A complement-microglial axis drives synapse loss during virus-induced memory impairment". Nature. 534 (7608): 538-543. Bibcode: ...
The scheme complements other initiatives taken by the government, for example Digital India, to benefit people by giving easier ... Khan, Danish (17 August 2016). "Electronic KYC to enable instant activation of mobile phone connections with Aadhar". The ...
Abramson, S.B., Belmont, H.M., Hopkins, P., Buyon, J., Winchester, R. and Weissmann, G. Complement activation and vascular ... he pioneered studies in both leukocyte activation (via complement component 5a, immune complexes, etc.), and the role of ... His laboratory found that crises in systemic lupus erythematosus are provoked by intravascular complement activation. Using a ... Goldstein, I.M., Roos, D., Kaplan, H., and Weissmann, G., Complement and immunoglobulins stimulate superoxide production by ...
... typically through voice activation. On most devices, the digital assistant can be activated by a dedicated button, or existing ... were discussed in a 2019 policy paper and two complements under the title "I'd blush if I could: Closing gender divides in ...
Next-generation sequencing is well suited in complementing bisulfite sequencing in genome-wide methylation analysis. While this ... From these studies, inferences on the function of histone modifications were made; that transcriptional activation or ... it is associated with gene activation but the opposite is found when it is within the promoter region. Histone modifications ... phosphorylation and ubiquitination have been implicated in gene activation whereas methylation, ubiquitination, SUMOylation, ...
"Activation/division of lymphocytes results in increased levels of cytoplasmic activation/proliferation-associated protein-1: ... Katsafanas GC, Moss B (December 2004). "Vaccinia virus intermediate stage transcription is complemented by Ras-GTPase- ... activating protein SH3 domain-binding protein (G3BP) and cytoplasmic activation/proliferation-associated protein (p137) ...
... regulate a diverse set of intracellular and extracellular processes such as complement activation, fibrinolysis, coagulation, ...
There is no thermal activation energy for the transformation from austenite to martensite.[clarification needed] There is no ... Another 19th-century steelmaking process was the Siemens-Martin process, which complemented the Bessemer process. It consisted ...
From their study of 58 patients, they found that immunoglobin M (IgM), complement, and fibrinogen were in the blood vessels of ... Later, these authors found data suggesting that activation of macrophages and fibroblasts are involved in the pathogenesis of ...
It had one activation zone for the race: on the straight between the Mandarin Oriental Bend and Lisboa corners. Per the ... An electronic flag system was implemented and elevated for the first time in ten areas of the circuit to complement the ... prompting the brief activation of the virtual safety car procedure to temporarily stop racing and allow for the recovery of ...
Both dusts consumed hemolytic complement and reduced the C3 complement, but the untreated dust was much more active than th ... The potential of cardroom cotton dust to activate in vitro the complement cascade from nonsensitized human and guinea pig sera ... The alternative pathway was identified as the source for complement activation. The authors suggest that the higher ... Cotton dust inhalation in vivo may induce airway changes mediated by complement activation. ...
The lectin pathway is one pathway of three by which the complement system is activated. The characteristic protease of this ... The complement system is an important immune mechanism mediating both recognition and elimination of foreign bodies. ... Simultaneous activation of complement and coagulation by MBL-associated serine protease 2 PLoS One. 2007 Jul 18;2(7):e623. doi ... The complement system is an important immune mechanism mediating both recognition and elimination of foreign bodies. The lectin ...
Complement activation-related pseudoallergy (CARPA) is a frequent side effect of intravenous therapies with nanoparticle- ... Activation of the complement system during and after cardiopulmonary bypass surgery: Postsurgery activation involves C-reactive ... Complement activation-related pseudoallergy (CARPA) is a frequent side effect of intravenous therapies with nanoparticle- ... Szebeni, J. (2005) Complement activation-related pseudoallergy: A new class of drug-induced acute immune toxicity. Toxicology, ...
... 2020-06-04T17:54:44Z. ... Fluoride Modification of Titanium Surfaces Enhance Complement Activation. Materials. 2020, 13(3), 684. ... The aim of the present study was to determine the ability of fluoride-modified titanium surfaces to activate complement ... Identification and quantification of complement cascade biomarkers were conducted using ELISA kits and multianalyte profiling ...
Complement activation in retinal degeneration. Citation. Rutar, M, Natoli, R, Provis, J et al 2012, Complement activation in ...
Watch this video to learn about the activation and biological functions of complement. ... The complement system is an important part of the innate immune response and plays a major role in the killing and clearance of ... Overview of Complement Activation and Biological Functions from Quidel Corporation. 13 March 2013 ... Watch this video to learn about the activation and biological functions of complement. ...
... Show full item record ... Reichhardt , M P & Meri , S 2016 , SALSA : A Regulator of the early Steps of Complement Activation on Mucosal Surfaces , ... Ulcerative colitis and Crohns disease are examples of diseases, where complement activation in mucosal tissues may occur. This ... Through these interactions SALSA regulates activation of the complement system. In addition, SALSA interacts with surfactant ...
Effects of complement activation products on the synthesis of decay accelerating factor and membrane cofactor protein by human ... Dive into the research topics of Effects of complement activation products on the synthesis of decay accelerating factor and ...
Correction: Systemic Complement Activation in Age-Related Macular Degeneration Scholl HPN., Charbel Issa P., Walier M., Janzer ...
Complement activation products were measured on serial blood samples obtained at each monthly visit. Results APO occurred in ... Complement activation products were measured on serial blood samples obtained at each monthly visit. Results APO occurred in ... Complement activation products were measured on serial blood samples obtained at each monthly visit. Results APO occurred in ... Complement activation products were measured on serial blood samples obtained at each monthly visit. Results APO occurred in ...
Complement activation in diabetic ketoacidosis and its treatment. Rita S. Jerath, C. Lynne Burek, William H. Hoffman, Gregory G ... Complement activation in diabetic ketoacidosis and its treatment. / Jerath, Rita S.; Burek, C. Lynne; Hoffman, William H. et al ... Complement activation in diabetic ketoacidosis and its treatment. Clinical Immunology. 2005 Jul;116(1):11-17. doi: 10.1016/j. ... Complement activation in diabetic ketoacidosis and its treatment. In: Clinical Immunology. 2005 ; Vol. 116, No. 1. pp. 11-17. ...
A complement cascade similar to that of the alternative pathway can be activated through specific antibody-antigen interactions ... ACTIVATION OF THE CLASSICAL COMPLEMENT PATHWAY. A complement cascade similar to that of the alternative pathway can be ... Activation of the Classical Complement Pathway. , Home , , Pharmaceutical Microbiology , , Pharmaceutical Microbiology , ... The presence of two complement pathways provides for rapid (alternative) and specific (classical) activation of a key defence ...
National Jewish Health Complement Laboratory performs a variety of complement activation tests for preclinical and clinical ... Complement Activation and Drug Development. Biopharmaceuticals or medical devices can cause off-target complement activation ... Advanced Diagnostic Laboratories offer a complete menu of tests that can be used to analyze complement activation in the pre- ... Complement Preclinical & Clinical Testing Services. * Clinical, in-vitro, and in-vivo complement studies, including access to a ...
... complement activation causes severe endplate membrane damage (45, 52). Brain biopsy findings support that complement activation ... Complement Activation. IgG1-3 can activate the complement system by forming the membrane attack complex (MAC) and leading to ... a water channel on astrocyte play a role in the pathology of NMO by triggering complement activation and ADCC (57). In vitro, ... Engel AG, Arahata K. The membrane attack complex of complement at the endplate in myasthenia gravisa. Ann N Y Acad Sci (1987) ...
A quantitative measurement of complement (C3) activation in severely burned patients. Journal of Burn Care and Rehabilitation. ... A quantitative measurement of complement (C3) activation in severely burned patients. In: Journal of Burn Care and ... Our findings confirm that both excessive C3 consumption and the low C3 activation rate may be observed among complement ... Our findings confirm that both excessive C3 consumption and the low C3 activation rate may be observed among complement ...
Investigating Complement receptors in non-immune cells pointed out Complement implication in the regeneration of tissue such as ... Cultured pulp fibroblasts secrete all Complement components. Complement C3b and MAC have been shown to control bacteria growth ... Complement activation links inflammation to dental tissue regeneration. ... Objectives: Complement is an efficient plasma immune surveillance system. It initiates inflammation by inducing vascular ...
Peptide Inhibitor of Complement C1 (PIC1) Rapidly Inhibits Complement Activation After Intravascular Injection In Rats. ... Inhibition of Complement Activation, Myeloperoxidase, NET Formation And Oxidant.... A product of rational molecular design, PA- ... Together these results show that PIC1 rapidly inhibits classical complement activation in vitro and in vivo and is functional ... Inhibition of Immune Complex Complement Activation And Neutrophil Extracellular.... Abstract: Two major aspects of systemic ...
Complement activation (fixation), in which antibodies that are latched onto a foreign cell encourage complement to attack it ... Activation of complementEdit. Antibodies that bind to surface antigens (for example, on bacteria) will attract the first ... these phagocytes are attracted by certain complement molecules generated in the complement cascade. Second, some complement ... component of the complement cascade with their Fc region and initiate activation of the "classical" complement system.[36] This ...
Complement factor C4 activation in patients with hereditary angioedema. By wil on March 13, 2018 in ... OBJECTIVES: Low complement factor C4 is usually considered a valuable screening tool for patients with the potentially life- ... Our aim was to investigate whether total antigenic C4 or non-functional C4c is a better measure of the increased C4 activation ... It has been suggested that measurement of C4 activation products is better suited to avoid false negative results. ...
Transcripts representing the classical complement pathway and Fcγ receptor 1 were also differentially expressed in the 12 mo ... We found transcripts representing the classical complement pathway and Fcγ receptor 1 overabundant from subclinical stages of ... Complement pathway gene activation and rising circulating immune complexes characterize early disease in HIV-associated ... Complement pathway gene activation and rising circulating immune complexes characterize early disease in HIV-associated ...
... hormonal changes and immunological activation. Recently, brain death has been shown to cause activation of the complement ... hormonal changes and immunological activation. Recently, brain death has been shown to cause activation of the complement ... hormonal changes and immunological activation. Recently, brain death has been shown to cause activation of the complement ... hormonal changes and immunological activation. Recently, brain death has been shown to cause activation of the complement ...
Parkash O, Ramanathan VD, Sengupta U. Use of immunofluorescence technique to demonstrate complement activation in vitro by ... Use of immunofluorescence technique to demonstrate complement activation in vitro by microbes. ...
Complement activation at the motor end-plates in amyotrophic lateral sclerosis. Overview of attention for article published in ... Here, we show that complement activation products and regulators are deposited on the motor end-plates of ALS patients. C1q co- ... This study provides evidence that complement activation products are deposited on innervated motor end-plates in the ... indicating that complement activation may precede end-plate denervation in human ALS. This study adds to the understanding of ...
Purchase Complement Regulatory Proteins - 1st Edition. Print Book & E-Book. ISBN 9780125069656, 9780080529561 ... The Complement System: A Brief Overview:. Introduction.. Activation of C.. Physiological Roles of C.. Involvement of C in ... Regulation in the Complement System:. Introduction.. History.. Control of Activation Pathways.. Control in the Membrane Attack ... Complement Regulatory Proteins in Other Species:. Introduction.. Regulators of the Activation pathways.. Regulators of the ...
Project: Influence of glycomic profiles in complement activation. External: The Wistar Institute and Penn Center for AIDS ... Project: Structure-activity relationships between liposomes and complement activation. External: University of Strathclyde. ... comlpement activation, platelet activation, coagulation), and cellular health (e.g., cytotoxicity, cell death pathways, ... Activation of immune cells, results in alteration of energy and nutrient requirements in order to provide sufficient energy ...
... positive regulation of complement activation, alternative pathway". ← Category:GO:0045958 ! positive regulation of complement ... The following pages link to Category:GO:0045958 ! positive regulation of complement activation, alternative pathway: View ( ... Category:GO:0044635 ! positive regulation of complement activation, alternative pathway in another organism ‎ (← links) ...
Complement. Promotes neutrophil and macrophage, platelet activation and chemotaxis, other proinflammatory effects ... Endothelial cell activation in emergency department patients with sepsis-related and non-sepsis-related hypotension. Shock. ... 91] Furthermore, catecholamine effectiveness on vascular smooth muscle cells is inhibited by the activation of ATP-dependent ... Activation of macrophages, neutrophils, platelets, and endothelium releases various cytokines and other mediators ...
Study shows complement activation plays an important role in inherited macular degeneration In a study published on line this ... complement system, a part of the immune system, prevented the disease. ...
In particular, this contact activation has implications for the therapeutic regulation of complement activation during liposome ... 2013 Mediation of a non-proteolytic activation of complement component C3 by phospholipid vesicles ... Liposome preparations have been described to activate complement. In this study, we have investigatedcomplement activation ... In addition, we demonstrated that DMPC liposomes bound to or were phagocytized by granulocytes in a complement-dependent manner ...
Allergic reactions to such PEGylated lipids can be IgE-mediated, but may also result from complement activation-related ... Possible involvement of polyethylene glycol and IgG-mediated complement activation. Klimek, Ludger; Novak, Natalija; Cabanillas ... Skin prick, intradermal and epicutaneous tests, in vitro sIgE assessment, evaluation of sIgG/IgM, and basophil activation tests ...
  • The alternative pathway was identified as the source for complement activation. (
  • The authors suggest that the higher concentration of endotoxin in the untreated dust cannot account for the total complement consumed, even though endotoxin activation of the alternative pathway has been documented. (
  • Conclusion In pregnant patients with SLE and/or aPL, increased Bb and sC5b-9 detectable early in pregnancy are strongly predictive of APOs and support activation of complement, particularly the alternative pathway, as a contributor to APOs. (
  • Results indicate that the alternative pathway may be the primary pathway of activation. (
  • A complement cascade similar to that of the alternative pathway can be activated through specific antibody-antigen interactions. (
  • Key steps in the activation of the classical pathway are shown in Figure 9.7, where this pathway is also compared to the alternative pathway. (
  • However, in contrast to the alternative pathway the activation step in the classical pathway requires specific antibody-antigen interactions. (
  • The functions of the classical complement pathway are similar to those described for the alternative pathway, i.e. opsonization, leucocyte activation and membrane lysis of target cells. (
  • Simple quantitative haemolytic microassay for determination of complement alternative pathway activation (AP50). (
  • INTRODUCTION: C3 glomerulopathy (C3G) is an ultrarare, chronic and progressive nephropathy mediated by dysregulation of the alternative pathway of complement (AP), with poor prognosis and limited treatment options. (
  • INTRODUCTION: C3 glomerulopathy (C3G) is a rare, progressive kidney disease resulting from dysregulation of the alternative pathway (AP) of complement. (
  • The lectin pathway is one pathway of three by which the complement system is activated. (
  • The characteristic protease of this pathway is Mannan-binding lectin (MBL)-associated serine protease 2 (MASP2), which cleaves complement proteins C2 and C4. (
  • One of the mucosal proteins known to interact with the early complement components of both the classical and the lectin pathway is the salivary scavenger and agglutinin (SALSA). (
  • The antibodies that activate the classical complement pathway are IgM and IgG. (
  • The classical pathway can additionally lead to complement protein deposition on insoluble antibody- antigen immune complexes circulating within blood, and in doing so promote the clearance of such potentially harmful complexes by Kupffer cells of the liver. (
  • Complement pathway gene activation and rising circulating immune complexes characterize early disease in HIV-associated tuberculosis. (
  • We found transcripts representing the classical complement pathway and Fcγ receptor 1 overabundant from subclinical stages of disease. (
  • Transcripts representing the classical complement pathway and Fcγ receptor 1 were also differentially expressed in the 12 mo before disease presentation. (
  • We describe right here a easy, dependable and quantitative methodology to measure the choice pathway (AP) dependent mode of complement activation for the lysis of rabbit erythrocytes. (
  • To make sure inhibition of the classical pathway of activation. (
  • the classical pathway initiated by antibodies bound to the surface of foreign bodies and the alternative and lectin pathways that provide an antibody-independent mechanism for complement activation, induced by the presence of bacteria and other micro-organisms. (
  • Mannan-binding lectin (MBL) and MBL-associated serine proteases (MASPs) are involved in the initial step of the lectin pathway of complement activation. (
  • Following these cleavage events, complement pathway activation continues as in the classical pathway. (
  • The complement component 2 protein is involved in the pathway that turns on (activates) the complement system when foreign invaders, such as bacteria, are detected. (
  • A lack of this protein impairs activation of the complement pathway. (
  • In other experiments, it was demonstrated that schistosomula, in the presence of IgG, were able to initiate complement activation also through the classical pathway (CP). (
  • The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. (
  • 18 Genetic or pharmacologic blockade of the complement pathway can prevent synaptic stripping and alleviate multiple age- and inflammation-related disorders. (
  • CAD is a type of autoimmune hemolytic anemia in which patients experience chronic hemolysis brought about by the activation of the classical component pathway, said corresponding author Alexander Röth, PhD, of the University of Duisburg-Essen, in Germany, and colleagues. (
  • Sutimlimab is a humanized monoclonal antibody targeting the complement-specific serine protease C1s, which activates the classical component pathway, leading to hemolysis. (
  • Most patients with atypical HUS have mutations in one or more of the genes that encode proteins involved in the alternate pathway of complement, which creates a predisposition to the disorder. (
  • Here, the complement proteins interact with other endogenous molecules to keep microbes from entering the parenteral tissues. (
  • Results: Recent data reported expression of Complement receptors and soluble proteins in dental tissues. (
  • From small beginnings in the early 1970s, the study of complement regulatory proteins has grown in the last decade to the point where it dominates the complement field. (
  • There are now more proteins known to be involved in controlling the complement system than there are components of the system and the list continues to grow. (
  • Many nanomaterials interact with serum proteins such as opsonins (e.g. antibodies, complement) and are rapidly taken up into cells of the mononuclear phagocyte system (e.g. macrophages). (
  • The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. (
  • These data further suggest that the organization of genes for functionally related proteins in clusters may be a rule for the complement system. (
  • The functions of complement include the attraction of inflammatory cells, opsonization to promote phagocytosis, immune complex clearance and direct microbial killing through the formation of the membrane attack complex (MAC). (
  • Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX . (
  • We investigated whether activation of complement early in pregnancy predicts APOs in women with systemic lupus erythematosus (SLE) and/or antiphospholipid (aPL) antibodies. (
  • C1q attaches to antibodies bound on the pathogen surface, leading to the activation of C1s. (
  • Blast TBI triggers an activation of the immune system, generation of auto- antibodies, as well as infiltration of circulating immune cells into the central nervous system (CNS). (
  • The potential of cardroom cotton dust to activate in vitro the complement cascade from nonsensitized human and guinea pig sera was investigated. (
  • Identification and quantification of complement cascade biomarkers were conducted using ELISA kits and multianalyte profiling using Luminex. (
  • We conclude that titanium surfaces treated with hydrofluoric acid modify the levels of specific biomarkers related to the complement cascade and angiogenesis and, thus, tissue growth, remodeling and repair, as this may play a role in the enhanced clinical performance of fluoride-modified Ti dental implants. (
  • C1 is the first molecule in the classical complement cascade and comprises C1q and two molecules of C1r and C1s respectively. (
  • The virus is taken up by dendritic cells, which, after antigen processing, presents it to T cells, leading to immune activation and release of a cascade of cytokines that are believed to mediate the systemic effects of plasma leakage and circulatory insufficiency. (
  • Blocks complement cascade. (
  • Activation of the complement cascade enhances motility of leukemic cells by downregulating expression of HO-1. (
  • Anaphylatoxins C3a and C5a are the strongest modulators produced by the complement cascade and can trigger cell activation and inflammatory signaling when binding to C3aR (C3a receptor) and C5aR (C5a receptor), which are considered emerging targets for therapeutic intervention in many diseases because the overexpression of C5aR and C3aR have shown to associated with many inflammatory conditions and neurological disorders. (
  • Antibody-independent complement activation by cardroom cotton dust. (
  • Role of complement and inhibition by soluble CR1 and anti-C5a antibody. (
  • Once this occurs, a complement protein termed C1 (which comprises a single C1q subunit, two C1r subunits and two C1s subunits) binds to adjacent Fc domains in the antibody-antigen complex. (
  • Further, when C1 is free in the circulation it is bound to a protein termed C1 inhibitor (C1-INH) which prevents any possible activation of C1 in the absence of antibody. (
  • This study investigated the effect of an inhibitory antibody against complement factor B on brain death-induced renal inflammation and injury. (
  • sB-1a cells resemble memory B2 cells, as they are stimulated within 1 h of immunization and depend on T helper cytokines-uniquely IL-4 from hepatic iNKT cells-for activation and rapid migration from the peritoneal cavity to the spleen to secrete IgM antibody (Ab) and Ab-derived free light chains (FLCs) by only 1 day after immunization. (
  • Biopharmaceuticals or medical devices can cause off-target complement activation that leads to destructive inflammation. (
  • It initiates inflammation by inducing vascular modifications and attracting immune cells expressing Complement receptors. (
  • Conclusions: Overall, this review highlights that local Complement synthesis in dental tissues plays a major role, not only in eliminating bacteria, but also in the initial steps of dental tissue regeneration, thus, providing a link between dental tissue inflammation and regeneration. (
  • Clinical relevance: Complement provides an explanation for understanding why inflammation preceeds regeneration. (
  • Many of the eosinophil mediators involved in the pathogenesis of airway inflammation are preformed and stored in granules that are released upon eosinophil activation. (
  • In addition, we demonstrated that DMPC liposomes bound to or were phagocytized by granulocytes in a complement-dependent manner, as evidenced by the use of complement inhibitors. (
  • Learn about the three pathways lead to complement activation and some of their key inhibitors. (
  • Providing custom inhibitors against various complement components based on specific project demands. (
  • Materials and methods: Review of literature was conducted on Complement local expression and implication in oral tissue regeneration in vivo and in vitro. (
  • To improve upon the solubility of the lead derivative, a pegylated, water soluble variant was developed, structurally characterized and demonstrated to inhibit complement activation in mouse plasma, as well as rat, non-human primate and human serum in vitro. (
  • Together these results show that PIC1 rapidly inhibits classical complement activation in vitro and in vivo and is functional for a variety of animal species, suggesting its utility in animal models of classical complement-mediated diseases. (
  • IMSEAR at SEARO: Use of immunofluorescence technique to demonstrate complement activation in vitro by microbes. (
  • Skin prick, intradermal and epicutaneous tests, in vitro sIgE assessment, evaluation of sIgG/ IgM , and basophil activation tests are being used to demonstrate allergic reactions to various components of the vaccines . (
  • A further complement protein, C2, binds to this membrane complex to give C4b2. (
  • This gene provides instructions for making the complement component 2 protein, which helps regulate a part of the body's immune response known as the complement system . (
  • The most common C2 gene mutation, which is found in more than 90 percent of people with complement component 2 deficiency, prevents the production of complement component 2 protein. (
  • Understanding how immune cells, autoantibodies, and complement protein affect eyes exposed to blast represents a critical knowledge gap. (
  • Despite the activation of Sukuk as a financing instrument since 2018, the interest in them clearly began during the current and preceding period, which justifies the extent to which companies need new liquidity methods in the light of the Coronavirus crisis. (
  • Investigating Complement receptors in non-immune cells pointed out Complement implication in the regeneration of tissue such as liver, skin or bone. (
  • They summarized research indicating that bats have immune elements found in most mammals, including pattern recognition receptors and multiple interferons, and show complement activity. (
  • Immediately after dental implant insertion, blood will be in direct contact and interact with the implant surface and activates inflammatory responses and complement cascades within seconds. (
  • The complement system has been increasingly recognized to play a pivotal role in a variety of inflammatory and autoimmune diseases. (
  • This process includes diffuse activation of inflammatory and coagulation cascades, vasodilation and vascular maldistribution, capillary endothelial leakage, and dysfunctional utilization of oxygen and nutrients at the cellular level. (
  • This clinical practice guideline complements the 2019 American College of Rheumatology JIA and uveitis guidelines, which addressed polyarthritis, sacroiliitis, enthesitis, and uveitis. (
  • Inhibition of Immune Complex Complement Activation And Neutrophil Extracellular. (
  • Inhibition of Complement Activation, Myeloperoxidase, NET Formation And Oxidant. (
  • Exsera for complement activation/inhibition & anaphylactoid. (
  • We excel in functional testing, activation, inhibition and multiplex analysis. (
  • Advanced Diagnostic Laboratories offer a complete menu of tests that can be used to analyze complement activation in the pre-clinical and clinical trial setting. (
  • Consequently, therapeutic modulators of the classical, lectin and alternative pathways of the complement system are currently in pre-clinical and clinical development. (
  • Complement and clinical biomarkers, biopsy composite score, and activity and chronicity indices were assessed at baseline and analyzed by pairwise Spearman correlation analysis. (
  • Thus, an alternative treatment that is non-cytotoxic, rapid, and durable in controlling classical complement-mediated hemolysis and its clinical manifestations in CAD patients is needed," the authors said. (
  • Recent clinical approval of the first compstatin-based C3-targeted therapeutic for PNH treatment and the approval of a small-molecule, C5aR1 antagonist, for severe ANCA-associated vasculitis, have enhanced researchers' confidence in the discovery of complement-targeted drugs. (
  • Both dusts consumed hemolytic complement and reduced the C3 complement, but the untreated dust was much more active than the treated dust. (
  • Our laboratory has identified a peptide that specifically inhibits the classical and lectin pathways of complement and is referred to as Peptide Inhibitor of Complement C1 (PIC1). (
  • To obtain a better understanding of the role of complement at the motor end-plates in human ALS pathology, we analyzed post-mortem tissue of ALS donors for complement activation and its regulators. (
  • Here, we show that complement activation products and regulators are deposited on the motor end-plates of ALS patients. (
  • High levels of the regulators CD55 and CD59 were detected at the motor end-plates of ALS donors but not in controls, suggesting an attempt to counteract complement activation and prevent MAC deposition on the end-plates before they are lost. (
  • The first few chapters discuss the "nuts-and-bolts" of the complement regulators, describing their structures, functional roles and modes of action. (
  • The roles of the complement regulators in vivo are then described, focusing on the consequences of deficiency, roles in the reproductive system, interactions with pathogens and exploitation for therapy. (
  • The interesting developments in defining the complement regulators expressed in other species are also discussed. (
  • Other Regulators of the Activation Pathways. (
  • Genetic variation in complement regulators and susceptibility to age-related macular degeneration. (
  • Low complement factor C4 is usually considered a valuable screening tool for patients with the potentially life-threatening hereditary angioedema with C1-inhibitor (C1-INH) deficiency (C1-INH-HAE). (
  • Complement component 2 deficiency is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. (
  • Complement component 2 deficiency is also associated with an increased risk of developing autoimmune disorders such as systemic lupus erythematosus (SLE) or vasculitis. (
  • Between 10 and 20 percent of individuals with complement component 2 deficiency develop SLE. (
  • Females with complement component 2 deficiency are more likely to have SLE than affected males, but this is also true of SLE in the general population. (
  • The severity of complement component 2 deficiency varies widely. (
  • Complement component 2 deficiency is caused by mutations in the C2 gene. (
  • It is unclear how complement component 2 deficiency leads to an increase in autoimmune disorders. (
  • It is likely that other factors, both genetic and environmental, play a role in the variability of the signs and symptoms of complement component 2 deficiency. (
  • According to the researchers, the method complements existing methods for phthalide synthesis. (
  • Atypical HUS may also be due to development of autoantibodies against complement factor H. (
  • Watch this video to learn about the activation and biological functions of complement. (
  • Assisting clients' sCR1 and CAB-2 projects based on a cutting-edge platform of soluble complement regulator services. (
  • In particular, this contact activation has implications for the therapeutic regulation of complement activation during liposome treatment. (
  • Embracing the promising roles of anaphylatoxin receptor antagonists in disease treatment, Creative Biolabs offers perfect anaphylatoxin receptor antagonist development services, as well as custom receptor antagonist development targeting a variety of complement components based on advanced development strategies and full-scale platforms, advancing the success of clients' complement therapeutic projects. (
  • For more information about complement therapeutic services at Creative Biolabs, please visit . (
  • The company upholds its extremely strict scientific awareness and is committed to delivering the best complement therapeutic services, which makes Creative Biolabs stand out as a premier CRO. (
  • Activation of these pathways could allow the burden of growth and organization of tissue to be handled by the limb itself, similar to how it occurs in an embryo, rather than require ongoing therapeutic intervention over the many months it takes to grow the limb. (
  • Studies in the SOD1(G93A) mouse show deposition of C1q and C3/C3b at the motor end-plate before neurological symptoms are apparent, suggesting that complement activation precedes neurodegeneration in this model. (
  • PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. (
  • The complement system is an important immune mechanism mediating both recognition and elimination of foreign bodies. (
  • Complement activation-related pseudoallergy (CARPA) is a frequent side effect of intravenous the rapies with nanoparticle-containing drugs and biologicals that are recognized by the immune system as foreign. (
  • The complement system is an important part of the innate immune response and plays a major role in the killing and clearance of bacteria, viruses, fungi and parasites. (
  • Through these interactions SALSA regulates activation of the complement system. (
  • The complement system is the innate immune system's first line of defense against infection. (
  • When the complement system becomes inappropriately activated - or when it does not activate as it should - serious health problems can result. (
  • Objectives: Complement is an efficient plasma immune surveillance system. (
  • Recently, brain death has been shown to cause activation of the complement system, which is adversely associated with renal allograft outcome in recipients. (
  • Modulation of the complement system in the brain-dead donor might be a promising strategy to improve organ quality before transplantation. (
  • anyone interested in the complement system. (
  • The complement system is a heat-labile component of blood that confers bactericidal properties. (
  • Researchers speculate that the dysfunctional complement system is unable to distinguish what it should attack, and it sometimes attacks normal tissues, leading to autoimmunity. (
  • Alternatively, the dysfunctional complement system may perform partial attacks on invading molecules, which leaves behind foreign fragments that are difficult to distinguish from the body's tissues, so the complement system sometimes attacks the body's own cells. (
  • Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. (
  • Several inherited deficiencies in the complement system occur in humans. (
  • OptiZinc ® + Quercetin provides critical immune system and antioxidant support to complement Vitamin D3's role in immune cell response. (
  • Complementing the infotainment system is the BMW Intelligent Personal Assistant, which can be activated by saying the phrase "Hey BMW" or any personal activation word. (
  • Thus, the aim of this work is to carry out a review of the literature on the role of bacterial endotoxin in the etiology of periapical lesions, its mechanism of action, and to elucidate molecular mechanisms involved in endotoxin's recognition by the immune system and cell activation. (
  • Therefore, the objective of this study is to carry out a review of the literature on the role of bacterial endotoxin in the etiology of periapical lesions, as well as to elucidate molecular mechanisms involved in its recognition by the immune system and in cell activation. (
  • Advanced Diagnostic Laboratories has a comprehensive menu of diagnostic tests that help clinicians determine whether complement defects or deficiencies are factors in patients with recurrent severe infections or symptoms of autoimmune disease. (
  • Ulcerative colitis and Crohn's disease are examples of diseases, where complement activation in mucosal tissues may occur. (
  • The new limbs had bone structure extended with features similar to a natural limb's bone structure, a richer complement of internal tissues (including neurons), and several "toes" grew from the end of the limb, although without the support of underlying bone. (
  • Results: Pretreatment with anti-FB resulted in significantly less systemic and local complement activation than in saline-treated rats after brain death. (
  • [ 3 ] For example, in pneumococcal HUS, S pneumoniae damages endothelial cells in the blood vessels, disturbing local complement homeostasis and producing a thrombogenic state. (
  • Physicochemical and functional characterization of the C1r subunit of the first complement component. (
  • Gender specific association of a complement component 3 polymorphism with polypoidal choroidal vasculopathy. (
  • Cotton dust inhalation in vivo may induce airway changes mediated by complement activation. (
  • M. and Barenholz, Y. (2007) Animal models of complement-mediated hypersensitivity reactions to liposomes and other lipid-based nanoparticles. (
  • The mechanisms of resistance were considered in terms of inherent hormone insensitivity, nonendocrine growth signalling, ER activation/hypersensitivity and inefficient/compromised therapy. (
  • Szebeni, J. (2005) Complement activation-related pseudoallergy: A new class of drug-induced acute immune toxicity. (
  • Allergic reactions to such PEGylated lipids can be IgE -mediated, but may also result from complement activation -related pseudoallergy (CARPA) that has been described in similar liposomes . (
  • We further analyzed the effect of arginine and glutamic acid residue substitution on the complement inhibitory activity of our lead derivative in a hemolytic assay and found that the original sequence demonstrated superior inhibitory activity. (
  • It has been suggested that measurement of C4 activation products is better suited to avoid false negative results. (
  • In all serum samples, the untreated dust consumed greater amounts of complement or complement components than the treated dust. (
  • The aim of the present study was to determine the ability of fluoride-modified titanium surfaces to activate complement cascades using the human buffy coat as model. (
  • Liposome preparations have been described to activate complement. (
  • In CS and DTH, sB-1a IgM Ag affinity is sufficiently high to mediate complement activation for generation of C5a that, together with vasoactive mediators such as TNF-α released by FLC-sensitized mast cells, activate local endothelium for extravascular recruitment of effector T cells. (
  • Complement C3 variant and the risk of age-related macular degeneration. (
  • Identification of a rare coding variant in complement 3 associated with age-related macular degeneration. (
  • Zinc supplementation inhibits complement activation in age-related macular degeneration. (
  • Les numérations plaquettaire et leucocytaire ainsi que la concentration en cytokines (IL-2R, IL-8 et TNF-) ont été me- surées. (
  • As a result, the complement system's ability to fight infections is diminished. (
  • It is involved in the activation of complement, enhancement of phagocytosis, and detoxification of substances released from damaged tissue. (
  • The authors are also appreciative of the expert secretarial support of Ms. C. Masters and acknowledge the staff in the Complement Laboratory at the National Jewish Medical and Research Center. (
  • Dr. Galvan serves as the Director of the Complement Laboratory. (
  • Our aim was to investigate whether total antigenic C4 or non-functional C4c is a better measure of the increased C4 activation in C1-INH-HAE patients. (
  • Plantapol Myrtirutin 20 ampoules it acts efficiently as a complement in the treatments that originate the activation and potentiation of blood circulation, the symptoms of menopause and improves cellulite. (
  • In brain death, the irreversible loss of brain functions results in hemodynamic instability, hormonal changes and immunological activation. (
  • There are stunning combinations that enable you to make a personal design statement and customize your faucet to match and complement other surfaces in your kitchen and home. (
  • The presence of two complement pathways provides for rapid (alternative) and specific (classical) activation of a key defence mechanism, and offers greater protection against the development of microbial resistance mechanisms. (
  • Human genes for three complement components that regulate the activation of C3 are tightly linked. (
  • 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. (
  • Benzamides, for example, are commonly used in C-H bond activation reactions, but only a few examples of this type of reaction between benzamides and aldehydes had been reported so far. (
  • The objectives of this study were to monitor the complement activation products C3a, C4a, Bb, and C5b-9 prior to, during, and after correction of DKA. (
  • This review will shed the light on its Complement implication in the initial steps of dental tissue regeneration. (
  • The specificity of the AP50 assay for AP complement activation was verified by the truth that a C4 affinity-depleted plasma gave an AP50 worth throughout the regular vary (52.eight U/ml) whereas the same aliquot of the identical plasma, affinity-depleted of issue B, gave an undetectable AP50 worth (lower than 10 U/ml). (