Chapter 2 Flashcards
All of the following statements are correct regarding \alpha2-macroglobulin except _____.
a. it binds covalently to its target via a thioester bond
b. it possesses a bait region to lure its target
c. it undergoes a conformational change that enables it to enshroud the target
d. when bound to its target it is cleared from the circulation by hepatocytes, fibroblasts, and macrophages bearing receptors specific for the complex
e. its target is the membrane-attack complex on human cells
its target is the membrane-attack complex on human cells
Which of the following are important in anchoring the membrane-attack complex to the membrane?
- C3 and C5
- C5 and C6
- C7 and C8
- C8 and C9
C7 and C8
The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are _____.
a. factor B and factor H
b. factor H and factor I
c. factor B and factor I
d. decay-accelerating factor and factor H
e. decay-accelerating factor and membrane cofactor protein
decay-accelerating factor and membrane cofactor protein
Which of the following does not describe the actions of the coagulation system?
a. blood clot formation
b. enhancement of dissemination of microbes into lymphatics and bloodstream
c. decrease in blood loss and fluid into interstitial spaces in tissues
d. release of inflammatory mediators by platelets
e. wound healing
enhancement of dissemination of microbes into lymphatics and bloodstream
Which of the following does not accurately describe complement components?
a. soluble proteins
b. made by the spleen
c. located in extracellular spaces
d. some function as proteases once activated
e. activated by a cascade of enzymatic reactions
made by the spleen
A genetic deficiency of C3 leads to a type of immunodeficiency characterized by recurrent and severe infections. 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. C3b becomes fixed to the pathogen surface and facilitates the opsonization of pathogens by phagocytes and the assembly of complement components for perforation of the pathogen membrane. In the absence of C3, all three pathways of complement activation would be arrested and extracellular pathogens would escape immune detection until adaptive immune mechanisms develop fully many days later.
True
Although activation of the three different pathways (alternative, lectin, and classical) of complement activation converge involves different components, the three pathways converge on a common enzymatic reaction referred to as complement fixation. The reaction involves the cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface.
True
G-protein-coupled receptors (CPCRs) for the anaphylatoxins C3a and C5a are found on phagocytes, mast cells, and the endothelial cells of blood vessel walls. Anaphylatoxin bound to mast cells causes them to degranulate, releasing inflammatory mediators such as histamine and leading to increased vascular permeability. Through their action on endothelial cells, anaphylatoxins exert vasoactive effects on blood vessels, contributing to increased vascular permeability and increased blood flow, which facilitate the extravasation of plasma proteins, such as complement proteins and antibodies, and the recruitment of cells to infected tissues through increased adherence and chemotaxis. Phagocytic activity is enhanced by anaphylatoxins, which bring about increased levels of CR1 and CR3 and microbicidal activity. All these activities enhance inflammation.
True
During the formation of the membrane-attack complex, it is important to expose the hydrophobic sites of C7 and C8, because these sites enable anchoring of these two complement components into the membrane of the pathogen. Once anchored in the membrane, the hydrophobic site of C8 facilitates C9 polymerization, which completes the formation of the membrane-attack complex.
True
Soluble effector molecules are effective when encountering pathogens in the body, except in/on _____.
a. extracellular spaces
b. cytoplasm
c. epithelial surfaces
d. interstitial spaces
e. vesicular compartments
cytoplasm
Which of complement pathway(s) becomes activated soonest after an initial infection?
a. The classical pathway
b. The lectin pathway
c. The alternative pathway
d. Both classical and alternative pathways
e. Both classical and lectin pathways
The alternative pathway
The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C3bBb), whereas the alternative pathway uses the alternative convertase (C4b2a).
False
C3 is the most abundant complement component in the plasma and circulates as a zymogen, an inactive enzyme. When cleaved into C3a and C3b, three different effector mechanisms are armed: (1) C3b binds to and tags pathogens for destruction by phagocytes through binding to a C3b receptor, CR1; (2) C3b contributes to a multicomponent enzyme, C5 convertase, that catalyzes the assembly of the terminal complement components and the formation of the membrane-attack complex; and (3) C3a is an inflammatory mediator that serves as a chemoattractant and recruits inflammatory cells to the infection site.
True
Anaphylatoxins C3a and C5a contribute physiologically to inflammation during complement activation. G-protein-coupled receptors for the anaphylatoxins C3a and C5a are found on phagocytes, mast cells, and the endothelial cells of blood vessel walls. Anaphylatoxin bound to mast cells causes them to degranulate, releasing inflammatory mediators such as histamine and leading to increased vascular permeability. Through their action on endothelial cells, anaphylatoxins exert vasoactive effects on blood vessels, contributing to increased vascular permeability and increased blood flow, which facilitate the extravasation of plasma proteins, such as complement proteins and antibodies, and the recruitment of cells to infected tissues through increased adherence and chemotaxis. Phagocytic activity is enhanced by anaphylatoxins, which bring about increased levels of CR1 and CR3 and microbicidal activity. All these activities enhance inflammation.
True
The steps that take place when a bacterium is opsonized via C3b:CR1 interaction between the bacterium and a resident macrophage in tissues are the following: (1) The CR1 on the macrophage can bind to C3b that is coating a bacterial surface after complement activation, and the macrophage then engulfs the bacterium through receptor-mediated endocytosis. (2) The macrophage membrane invaginates and forms an intracellular vesicle called a phagosome. (3) The phagosome fuses with a lysosome to form a phagolysosome, where toxic mediators and degradative enzymes are localized. (4) The bacterium is destroyed.
True
Which of the following does not describe defensins?
a. highly conserved with few variants
b. contain a large proportion of arginine residues
c. contain three intra-chain disulfide bonds
d. amphipathic, with hydrophobic and hydrophilic regions
e. disrupt pathogen membranes by penetrating them and disrupting their integrity
highly conserved with few variants
The plasma proteins that counteract the activity of factor P by inactivating C3 convertase through the cleavage of C3b are _____.
a. factor B and factor H
b. factor H and factor I
c. factor B and factor I
d. decay-accelerating factor and factor H
e. decay-accelerating factor and membrane cofactor protein
factor H and factor I
The alternative C3 convertase on pathogen cell surfaces is formed by spontaneous hydrolysis of C3 without cleavage exposes its highly reactive thioester bond, forming iC3. Factor B binds to iC3, is cleaved by factor D, and consequently releases a small fragment called Ba. The larger fragment, Bb, remains associated with iC3 to form iC3Bb, a soluble C3 convertase, which cleaves C3 into C3a and C3b. The reactive thioester bond of C3b is attacked by R OH and R NH2 groups on the surface of the pathogen, where it becomes anchored and binds to factor B. Factor D then cleaves factor B, releasing fragment Ba and forming C3bBb on the pathogen surface. The alternative C3 convertase on pathogen cell surfaces is stabilized by Factor P (properdin) binds to C3 convertase (C3bBb) bound to the pathogen surface, and inhibits the proteolytic degradation of C3bBb. This stabilizes the C3 convertase and enhances the rate of C3b deposition on the pathogen surface.
True
Only the classical pathway is considered part of the adaptive immune response because of the requirement for antibody. However, the classical pathway is also considered part of innate immunity because of the ability of C-reactive protein, an acute-phase protein, to activate it. The other two pathways are considered part of innate immunity because they are initiated independently of antibody.
True
Which of the following is the membrane-bound form of C3 convertase of the alternative pathway of complement activation?
a. iC3
b. C3a
c. C3b
d. iC3Bb
e. C3bBb
C3bBb
