c which of the following can activate the complement cascade in any of the three pathways?

Complement activation takes place through any of the following three pathways: The classical pathway The alternative pathway The lectin pathway The complement system is activated by microbes and by antibodies that are attached to microbes and other antigens. Classical pathway

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What are the three activation pathways of the complement cascade?

Mar 23, 2019 · Part C Which of the following can activate the complement cascade in any of the three pathways? View Available Hint(s) O C1, Lipid-carbohydrate complex, and mannose-binding lectin O Antibodies, factor B, and carbohydrate containing mannose O Antibodies, factor B, and mannose-binding lectin O C1, tactor B, and mannose-binding lectin Submit s Previous

What is complement cascade in biology?

There are three pathways of complement activation: the classical pathway, which is triggered directly by pathogen or indirectly by antibody binding to the pathogen surface; the MB-lectin pathway; and the alternative pathway, which also provides …

What is the complement system and how is it activated?

View Available Hint(s) C5 C3a C5b O C3b Submit Part C Which of the following can activate the complement cascade in any of the three pathways? View Available Hint(s) Antibodies, factor B, and carbohydrate containing mannose Antibodies, factor B, and mannose-binding lectin C1, factor B, and mannose-binding lectin C1, Lipid-carbohydrate complex, and mannose-binding lectin …

What is the classical complement pathway?

C3 is a key element in the initiation of the complement cascade in all three pathways of complement activation, namely the alternative, lectin, and classical pathways. Its cleavage into C3a and C3b occurs early in the complement cascade. C3a acts as an inflammatory mediator and recruits inflammatory cells to the site of infection.

What are the 3 pathways of complement activation?

The complement pathway. Complement can be activated through three pathways: classical, lectin, and alternative.Dec 15, 2009

Which substance activates the complement cascade?

The complement activation initiated by heat shock proteins can occur in the absence of pathogens. Therefore, even aseptic tissue injury activates the complement cascade. In addition, microbes and their shed or secreted products activate complement through binding to C1q or MBL.

Which pathway activates complement system?

The lectin pathway is one of three pathways by which the complement system can be activated. This pathway is initiated by the binding of mannose-binding lectin (MBL), collectin 11 (CL-K1), and ficolins (Ficolin-1, Ficolin-2, and Ficolin-3) to microbial surface oligosaccharides and acetylated residues, respectively.Jan 21, 2015

Which of the following is able to activate complement?

Proteins such as albumin, gamma globulin, fibrinogen, fibronectin, vitronectin, and complement are adsorbed onto the surface of the biomaterial and activate complement (Anderson et al., 2008). Activation of complement leads to the conversion of C3 to C3a and C3b by the enzyme C3 convertase, C3bBb.

How is the complement pathway activated?

The complement system activates through a triggered-enzyme cascade. In such a cascade, an active complement enzyme generated by cleavage of its zymogen precursor then cleaves its substrate, another complement zymogen, to its active enzymatic form.

What does the complement cascade do?

The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.

When is complement system activated?

The complement system plays a critical role in inflammation and defence against some bacterial infections. Complement may also be activated during reactions against incompatible blood transfusions, and during the damaging immune responses that accompany autoimmune disease.

How is the complement system activated quizlet?

-Activation of the complement system can be initiated in several different ways: classical pathway, alternative pathway, and lectin pathway. ... Split products generated during complement activation promote inflammation. -MAC (membrane attack complexes): Lysis of the foreign cells and bacteria.

Which of the following complement pathways triggers the cleavage of C3 to C3a and C3b?

C3 Convertase activates C3 by splitting it into C3a and C3b.

Which of the following proteins of the complement cascade is an Opsonin?

C3b, C4b, and C1q are important complement proteins that mediate opsonization. As a part of the alternative complement pathway, the spontaneous activation of a complement cascade converts C3 to C3b, a component that can serve as an opsonin when bound to an antigen's surface.

Which of the following immunoglobulins is able to activate complement?

IgM is specialized to activate complement efficiently upon binding antigen. IgG antibodies are usually of higher affinity and are found in blood and in extracellular fluid, where they can neutralize toxins, viruses, and bacteria, opsonize them for phagocytosis, and activate the complement system.

Which of the following is required for C1 activation?

C1 activation, which is accompanied by limited proteolysis and conformational changes, can be induced by immune complexes or certain nonimmune substances. With C1 binding to an immune complex, the strength of interaction between C1q and C1r2s2 increases.

Which pathways activate the complement system select all that apply?

The classical pathway for activation of the complement cascade is triggered by the presence of IgG or IgM antigen-antibody complexes. Activation of C3 initiates the alternative pathway. Inflammation does not initiate the classical pathway, but instead inflammation is enhanced by the complement cascade.

Which complement protein is the product of all 3 activation pathways?

Complement Activation during Normal Homeostasis and Pathogen Infection. The central component of the complement system is C3. The activation of each of the three pathways (CP, LP, and AP) results in cleavage of inactive C3 protein into the functional fragments C3a and C3b.Jun 2, 2015

Which substance activates the complement cascade?

The complement activation initiated by heat shock proteins can occur in the absence of pathogens. Therefore, even aseptic tissue injury activates the complement cascade. In addition, microbes and their shed or secreted products activate complement through binding to C1q or MBL.

What activates complement system?

The complement pathway. Complement can be activated through three pathways: classical, lectin, and alternative. The classical pathway is activated when C1q binds to antibody attached to antigen, activating C1r and C1s, which cleave C4 and C2.Dec 15, 2009

How is complement cascade activated?

The complement system activates through a triggered-enzyme cascade. In such a cascade, an active complement enzyme generated by cleavage of its zymogen precursor then cleaves its substrate, another complement zymogen, to its active enzymatic form.

What does the complement cascade do?

The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.

Which of the following proteins of the complement cascade is an Opsonin?

C3b, C4b, and C1q are important complement proteins that mediate opsonization. As a part of the alternative complement pathway, the spontaneous activation of a complement cascade converts C3 to C3b, a component that can serve as an opsonin when bound to an antigen's surface.

What is complement system?

The complement system is a part of the innate immune system, consists of a series of proteins that interact with one another in a highly regulated manner, in order to eliminate pathogens. It helps antibodies and phagocytic cells to clear pathogens and damaged cells; promote inflammation and attack ...

How does complement activation work?

Complement activation is triggered by an antibody when it is bound to the antigen. It can also be triggered by some components of innate immunity. Thus the complement system works in both innate and acquired immunity. Complements are activated only during inflammatory reactions.

What is the MBL pathway?

The lectin recognizes and binds the carbohydrate of the target cell which then activates complements. MBL pathway resembles classical pathway as it proceeds through the action of C4 and C2 to produce activated proteins of the complement system. MBL works same as C1q which it resembles in structure. After the MBL binds to carbohydrate residues on ...

What is the function of complement proteins?

Immune clearance. The complement system removes immune complexes from the circulation and deposits them in the spleen and liver. Thus it acts as anti-inflammatory function. Complement proteins promote the solubilization of these complexes and their clearance by phagocytes.

What is the C1 complex?

C1 is a large, multimeric, protein complex composed of one molecule of C1q and two molecules each of C1r and C1s subunits. C1q binds to the antigen bound antibody (Fc portion). C1r and C1s are proteases which help to cleave C4 and C2.

What is the cause of lupus erythematosus?

Deficiency of C2 and C4 can cause systemic lupus erythematosus; deficiency of C3 and factor D can cause pyogenic bacterial infection; and deficiency of C5-C9 (or MAC deficiency) may lead to Neisserial infections like, gonorrhea and meningitis.

Why is classical complement important?

Complement is responsible for immune inflammatory response in adipose tissues which has been implicated in the development of obesity.

What is the binding of C1q?

The binding of C1q leads to conformational changes and the activation of the serine protease C1r. The activated C1r then cleaves and activates the serine protease C1s. The activated C1s cleaves C4 into C4a and C4b, and C2 into C2a and C2b. The larger fragments C4b and C2b form C4b2b (according to old terminology, C2a and C4b2a), a C3 convertase of the classical pathway. C3 convertase then cleaves C3 into C3a and C3b. While the anaphylatoxin C3a interacts with its C3a receptor (C3aR) to recruit leukocytes, C3b contributes to further downstream complement activation.

How do immunotherapies work?

Immunotherapies have been developed to detect and destroy cells infected by the HIV virus via classical complement activation. This process involves creating synthetic peptides that target conserved regions in HIV specific proteins and induce an antibody specific immune response through IgG antibodies.

Does obesity cause inflammation?

Obesity in turn results in an abnormally high level of complement activation via production of the C1 component of the classical pathway, which can lead to tissue inflammation and eventually insulin resistance, however the exact mechanisms that causes this is yet unknown.

What is a cinryze?

Cinryze, a human plasma derived C1-esterase inhibitor, has been approved for use in 2008 for the prevention of hereditary angioedema attacks. Deficiency in the C1q protein of the classical complement pathway can lead to development of systemic lupus erythematosus.

What is C1Q in Lupus?

Among the many functions of C1q, C1q triggers clearance of immune complexes and apoptotic cells by activating the classical pathway and binding directly onto phagocytes . Consequently, systemic lupus erythematosus from insufficient amounts of C1q is characterized by the accumulation of autoantibodies and apoptotic cells.

What is the C5A receptor?

Like C3a, C5a is also an anaphylatoxin that interacts with its cognate C5a receptor ( C5aR) to attract leukocytes. Subsequent interactions between C5b and other terminal components C6, C7, C8, and C9 form the membrane attack complex or the C5b-9 complex which forms pores on the target cell membranes to lysing.

What is complement cascade?

The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, ...

How is the complement system regulated?

The complement system is regulated by complement control proteins, which are present at a higher concentration in the blood plasma than the complement proteins themselves.

What are the components of the complement system?

About 50 proteins and protein fragments make up the complement system, including serum proteins, and cell membrane receptors. They account for about 10% of the globulin fraction of blood serum. Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway, and the lectin pathway.

What is the killing property of sheep blood?

In 1891, Hans Ernst August Buchner, noting the same property of blood in his experiments, named the killing property "alexin", which means "to ward off" in Greek. By 1894, several laboratories had demonstrated that serum from guinea pigs that had recovered from cholera killed the cholera bacterium in vitro. Heating the serum destroyed its killing activity. Nevertheless, the heat-inactivated serum, when injected into guinea pigs exposed to the cholera bacteria, maintained its ability to protect the animals from illness. Jules Bordet, a young Belgian scientist in Paris at the Pasteur Institute, concluded that this principle has two components, one that maintained a "sensitizing" effect after being heated and one (alexin ) whose toxic effect was lost after being heated. The heat-stable component was responsible for immunity against specific microorganisms, whereas the heat-sensitive component was responsible for the non-specific antimicrobial activity conferred by all normal sera. In 1899, Paul Ehrlich renamed the heat-sensitive component "complement."

What is the alternative complement pathway?

Accordingly, the alternative complement pathway is one element of innate immunity. Once the alternative C3 convertase enzyme is formed on a pathogen or cell surface, it may bind covalently another C3b, to form C3bBbC3bP, the C5 convertase. This enzyme then cleaves C5 to C5a, a potent anaphylatoxin, and C5b.

What is the lectin pathway?

The lectin pathway is homologous to the classical pathway, but with the opsonin, mannose-binding lectin (MBL), and ficolins, instead of C1q. This pathway is activated by binding of MBL to mannose residues on the pathogen surface, which activates the MBL-associated serine proteases, MASP-1, and MASP-2 (very similar to C1r and C1s, respectively), which can then split C4 into C4a and C4b and C2 into C2a and C2b. C4b and C2b then bind together to form the classical C3-convertase, as in the classical pathway. Ficolins are homologous to MBL and function via MASP in a similar way. Several single-nucleotide polymorphisms have been described in M-ficolin in humans, with effect on ligand-binding ability and serum levels. Historically, the larger fragment of C2 was named C2a, but it is now referred to as C2b. In invertebrates without an adaptive immune system, ficolins are expanded and their binding specificities diversified to compensate for the lack of pathogen-specific recognition molecules.

What is the larger fragment of C2?

Historically, the larger fragment of C2 was named C2a, but it is now referred to as C2b. In invertebrates without an adaptive immune system, ficolins are expanded and their binding specificities diversified to compensate for the lack of pathogen-specific recognition molecules.

What is the immune response to biomaterials?

The immune response to a biomaterial involves both humoral and cellular components. Activation of the complement cascade by either classical, lectin or alternative pathways leads to the deposition of C4b and C3b proteins. Recognition of these molecules by receptors on granulocytes can cause activation of these cells, leading to the production of degradative enzymes and destructive oxygen metabolites. Recognition of C4b or C3b by other proteins in the cascade leads to enzyme formation (C3 and C5 convertases), which amplifies the response and can lead to the production of a potent inflammatory mediator, C5a. C5a binds to specific receptors found on PMNs and monocytes. The interaction of C5a with these cells elicits a variety of responses, including hyperadherence, degranulation, superoxide production, chemotaxis, and cytokine production. Systemic exposure to C5a during extracorporeal therapies has been associated with neutropenia and cardiopulmonary manifestations (Tables II.2.4.9 and II.2.4.10) that can have pathologic consequences. The other portion of the C5 protein, C5b, leads to formation of a membrane attack complex that activates cells at sublytic levels and has cytotoxic potential if produced in large amounts. The control of these processes is understood well enough to begin designing materials that are more biocompatible. Limiting C3b deposition (nucleophilicity), adsorbing C5a to negatively charged surface groups, and facilitating the role of factors H and I are three approaches that have been shown to be effective. Translating the last mechanism into commercial materials is one of the major challenges facing the development of truly complement-compatible membranes.

What is the function of complement cascade?

The basic functions of the complement cascade are to recruit effector phagocytes for opsonization and clearance of foreign pathogens as well as trigger direct destruction of the foreign organism. Activation of the cascade proceeds by three different stimuli.

What is ahus in a patient?

aHUS is a rare, serious condition characterized by thrombotic microangiopathy and acute renal insufficiency. It is caused by the uncontrolled activation of the complement cascade, with mutations in key regulators of the complement cascade occurring in about 50% of aHUS patients (Caprioli et al., 2006 ). Due to the role of complement activation in the genesis of aHUS, the use of Ecu has been advocated for treatment of this condition ( Brown et al., 2007 ). The amelioration of glomerulonephritis induced by BB5.1 in knockout mice for factor H, an experimental model of aHUS, provided the first proof of concept in favor of this approach ( Pickering et al., 2006 ). In 2009, two case reports were published showing for the first time in humans that serious aHUS can be effectively managed with Ecu ( Nürnberger et al., 2009; Gruppo and Rother, 2009 ). The results of phase 2 clinical trials showed both in adults and in adolescents with aHUS a substantial increase in renal function and platelet count, a decrease in the frequency of thrombotic events and an improvement in quality of life ( Legendre et al., 2013 ). In September 2011, Ecu received fast track approval for aHUS and in 2014 the approval was converted to regular on the basis of further clinical evidence of efficacy in this disease.

What is complement activation?

Complement activation following implantation of biomaterials occurs in response to a number of current medical treatments, including but not limited to, insertion of catheters, prostheses, stents, and grafts. The complement cascade is a network of plasma proteins and cell surface receptors that recognize non-self-components and triggers one of the three pathways. An antigen–antibody complex triggers the classical pathway; carbohydrates trigger the lectin pathway; and foreign surfaces trigger the alternative pathway. Biomaterials, as one might expect, act primarily upon the alternative pathway. An important mediator of complement activation is the instant blood-mediated inflammatory reaction. The injury caused by surgical trauma leads to activation of the clotting cascade and endogenous upregulation of IgG and IgM, which then triggers complement, chondroitin sulfate, and tissue factor (Nilsson et al., 2010 ). Proteins such as albumin, gamma globulin, fibrinogen, fibronectin, vitronectin, and complement are adsorbed onto the surface of the biomaterial and activate complement ( Anderson et al., 2008 ). Activation of complement leads to the conversion of C3 to C3a and C3b by the enzyme C3 convertase, C3bBb. The subsequent amplification loop generates the bulk of C3 activation. C3b can also bind covalently to cells, or other materials, triggering opsonization by macrophages and other phagocytic cells that express complement receptors. Further convertases then catalyze the conversion of C5 into C5a and C5b. C3a and C5a are potent anaphylatoxins, mediating acute inflammatory reactions. The final product of the complement pathway is the membrane attack complex comprising C5b–C59, which then punctures holes in the cell membrane thereby facilitating killing of foreign pathogens ( Ricklin et al., 2010 ).

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