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Flashcards in Chapter 2 quiz Deck (20):
1

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

c. The alternative pathway

2

_____ are soluble complement fragments that mediate localized and systemic inflammatory responses.

a. cryptdins
b. defensins
c. anaphylatoxins
d. selectins
e. C-reactive proteins

c. anaphylatoxins

3

( T or F) 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

4

(T or F) 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

5

(T or F) 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

6

(T or F) 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

7

(T or F) Regarding the three pathways of complement: (1) The classical pathway requires an activating surface of a pathogen, which stabilizes complement components. (2) The lectin pathway requires the presence of mannose-binding lectin, an acute-phase protein made by the liver in response to interleukin-6 (IL-6) (secreted by activated macrophages) and which accumulates in plasma during infection. (3) The alternative pathway is activated in two ways, either by the presence of antibody bound to the surface of the microorganism (for example IgM bound to lipopolysaccharide of Gram- negative bacteria) or by the presence of C-reactive protein bound to a bacterium.

False

8

(T or F) 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

9

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

b. made by the spleen

10

(T or F) 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

11

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

e. C3bBb

12

(T or F) 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

13

(T or F) 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

14

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

b. factor H and factor I

15

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

e. decay-accelerating factor and membrane cofactor protein

16

(T or F) 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

17

Which of the following polymerizes to form a transmembrane channel that compromises the integrity of cell membranes?

a. C5
b. C6
c. C7
d. C8
e. C9

e. C9

18

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

b. enhancement of dissemination of microbes into lymphatics and bloodstream

19

Damage to tissues triggers a cascade of plasma proteins involving bradykinin and is known as _____.

a. the alternative pathway of complement
b. the coagulation system
c. the kinin system
d. receptor-mediated endocytosis
e. the acute-phase response

c. the kinin system

20

Which of the following complement components is an opsonin that binds to complement receptor 1 (CR1) on macrophages?

a. C3b
b. C3a
c. Bb
d. Ba
e. C3bBb

a. C3b