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Transcript
full file at http://testbankcorner.eu
THE IMMUNE SYSTEM, FOURTH EDITION
CHAPTER 9: IMMUNITY MEDIATED BY B CELLS AND
ANTIBODIES
© Garland Science 2015
9–1
a.
b.
c.
d.
e.
Which of the following is not a function of antibodies?
They neutralize pathogens by masking their surface.
They act as molecular adaptors that bridge together pathogen and phagocyte surfaces.
They exert toxic effects directly.
They act as opsonins that mediate phagocytosis.
They activate complement fixation.
9–2 To mount the most effective antibody response that results in the synthesis of highaffinity antibodies, which of the following must occur? (Select all that apply.)
a.
recognition of thymus-independent (TI) antigens
b.
isotype switching
c.
increased expression of TLR9 by B cells
d.
affinity maturation
e.
decreased expression of CD40 by B cells.
9–3
a.
b.
c.
d.
e.
Immunoreceptor tyrosine-based activation motifs (ITAMs) are located on _____.
the cytoplasmic tails of IgM
tyrosine kinases Blk, Fyn, and Lyn
the cytoplasmic tails of Igα and Igβ
breakdown products of C3b deposited on pathogen surfaces
thymus-independent antigens.
9–4
a.
b.
c.
d.
e.
f.
Identify the mismatched association.
Syk: Igβ cytoplasmic tails
tyrosine kinase Lyn: CD81
B-cell co-receptor: CD21/CD19/CD81
C3b fragments: C3d and iC3b
C3b/CR1: factor I
hyper-IgM syndrome: CD40 ligand deficiency.
9–5 A primary focus of clonal expansion is best described as _____.
a.
the location in the B-cell zone where conjugate pairs of B and T cells undergo cellular
proliferation, isotype switching, and somatic hypermutation
b.
the location in the medullary cords where conjugate pairs of B cells and T cells undergo
cellular proliferation and IgM is secreted
c.
the dark zone of the germinal center where centroblasts divide and pack closely together
d.
the initial wave of B-cell proliferation induced by T-independent antigens.
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full file at http://testbankcorner.eu
9–6 A primary focus forms after a circulating naive B cell forms a conjugate pair with _____
in the _____ of a lymph node.
a.
TH1 cell; B-cell zone
b.
cytotoxic T cell; T-cell zone
c.
follicular dendritic cell; germinal center
d.
TFH; medullary cords
e.
CD40 ligand; T-cell zone.
9–7 Which of the following do not bind to components found on the surface of an activated B
cell? (Select all that apply.)
a.
MHC class II
b.
T-cell receptor
c.
antigen
d.
CD40
e.
C3d
f.
IL-4
g.
CD4
h.
LFA-1
i.
CD40 ligand.
9–8 B cells migrating directly from a primary focus to the medullary cords in a lymph node
after activation with a T-dependent antigen differentiate into plasma cells that secrete
predominantly _____.
a.
IgD
b.
IgE
c.
sIgA
d.
IgG
e.
IgM.
9–9 Lymphoblasts upregulate a transcription factor called _____ when they terminally
differentiate into plasma cells.
a.
NFκB
b.
Bcl-xL
c.
B-lymphocyte induced maturation protein 1 (BLIMP-1)
d.
CD40
e.
ICAM-1.
9–10 The primary focus of B-cell expansion forms in the _____, whereas a secondary focus of
B-cell expansion creates the _____.
a.
T-cell area; medullary cords
b.
medullary cords; T-cell area
c.
T-cell area; B-cell area
d.
medullary cords; germinal center
e.
light zone; dark zone.
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full file at http://testbankcorner.eu
9–11 Proliferating centroblasts use the DNA-modifying enzyme activation-induced cytidine
deaminase for ________. (Select all that apply.)
a.
cell proliferation
b.
somatic hypermutation
c.
apoptosis
d.
upregulation of CD40
e.
isotype switching.
9–12 What is the fate of centrocytes in which somatic hypermutation has resulted in highaffinity receptors for antigen? (Select all that apply.)
a.
They die by apoptosis.
b.
They express Bcl-xL.
c.
They process antigen and present it to TFH cells.
d.
CD40 on the centrocyte engages with CD40 ligand on TFH cells.
e.
They undergo phagocytosis by tingible body macrophages.
9–13
a.
b.
c.
d.
e.
The main function of Bcl-xL is to _____ in the centrocyte.
provide death signals
induce somatic hypermutation
upregulate the expression of activation-induced cytidine deaminase
prevent apoptosis
induce isotype switching.
9–14
a.
b.
c.
d.
e.
Engulfment of apoptotic centrocytes is facilitated by _____ in germinal centers.
follicular dendritic cells
immune-complex coated bodies (iccosomes)
tingible body macrophages
antigen-specific B cells
antigen-specific TFH cells.
9–15 Match the term in column A with its description in column B.
Column A
Column B
1. expressed in centrocytes and prevents
___a. CCP modules
apoptosis
2. associated with the development of swollen
___b. ICAM-1
lymph nodes
3. required to induce production of activation___c. CR2
induced cytidine deaminase
4. expressed on B cells, follicular dendritic
___d. BLIMP-1
cells, and subcapsular sinus macrophages and
binds C3d
5. CR2-associated and needed for binding to
___e. CD40 ligand
C3d-tagged antigens
6. controls lymphoblast differentiation by
___f. Bcl-xL
acting as a transcription factor
7. binds to LFA-1 on T cells and fortifies
___g. germinal center reaction
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full file at http://testbankcorner.eu
___h. CD69
cognate B–T interactions
8. early indicator of B-cell activation and
repressor of SIP receptor expression
9–16 Which of the following is an accurate description of how centroblasts differ from
centrocytes?
a.
Centroblasts cease their expression of cell-surface immunoglobulins.
b.
Centroblasts divide more slowly than centrocytes.
c.
Centroblasts express CD44 but centrocytes do not.
d.
Centrocytes, but not centroblasts, initiate the process of isotype switching.
e.
Centroblasts participate in affinity maturation.
9–17 If a centrocyte does not interact with antigen and engage CD40 shortly after its
derivation, then _____.
a.
it recommences somatic hypermutation
b.
it undergoes apoptosis
c.
it moves back into the dark zone of the germinal center and switches its isotype
d.
its surface immunogloblulin levels decrease and proliferation recommences.
9–18 _____ is a mechanism that drives the preferential selection of immunoglobulins with the
highest affinity for antigen.
a.
Anergy
b.
Isotype-switching
c.
Affinity maturation
d.
Antibody-dependent cell-mediated cytotoxicity
e.
Transcytosis.
9–19 Match the cell type found in the lymph node in column A with its description in column
B.
Column A
Column B
1. not bone marrow-derived hematopoietic
___a. centroblast
cells
2. engulf apoptotic centrocytes
___b. tingible body macrophage
3. undergo somatic hypermutation
___c. naive B cell
4. make up the mantle zone
___d. follicular dendritic cells (FDC)
5. differentiate under the influence of an IL-4___e. memory B cell
secreting TFH cell
9–20 _____ in the switch regions positioned 5′ to each heavy-chain C gene is induced by
_____.
a.
Somatic hypermutation; TI antigens
b.
Chromatin remodeling; B-cell co-receptor signaling
c.
Recombination; survival signals received from follicular dendritic cells
d.
Transcription; helper T-cell cytokines
e.
Gene repression; apoptotic signals received from tingible body macrophages.
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full file at http://testbankcorner.eu
9–21
a.
b.
c.
d.
Plasma cells and memory B cells differentiate most immediately from _____.
centrocytes
centroblasts
B-1 cells
IgG-secreting B cells.
9–22 Which of the following statements is true regarding the complement component C4B?
a.
Deficiency of C4B is associated with systemic lupus erythematosus (SLE).
b.
C4B has similar properties to those of C4A.
c.
The thioester bond of C4B is preferentially acted upon by amino groups of
macromolecules.
d.
C4B is encoded in the class II region of the MHC.
e.
The gene for C4B is duplicated or deleted in some individuals.
9–23
a.
b.
c.
d.
e.
f.
g.
Which of the following is able to bind to C1q? (Select all that apply.)
bacterial adhesins
toxoids
IgM
C-reactive protein
hemagglutinin
lipopolysaccharide
classical C3 convertase.
9–24
a.
b.
c.
d.
e.
IgM is particularly efficient at fixing complement because it _____.
is a much larger antibody than the other isotypes
has an extra CH domain
is made first in an immune response and therefore has first access to C1q
has five binding sites for C1q
has easy access to extravascular areas.
9–25 C3 convertase of the classical pathway is _____, whereas C3 convertase of the alternative
pathway is _____.
a.
C1a; C3bBb
b.
C4bC2a; C3bBb
c.
C3bCR1; C3bBb
d.
C4bC2a; C3bCR1
e.
C1a; C3bCR1.
9–26 Which of the following statements are true regarding C4? (Select all that apply.)
a.
There are two forms of C4 encoded by separate genes residing in the class II region of the
MHC.
b.
Evolution of the different forms of C4 probably occurred as a result of gene duplication
and diversification.
c.
Because there are two forms of C4, C4 deficiency is the least common human
immunodeficiency.
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full file at http://testbankcorner.eu
d.
More than 30% of the human population lacks either C4A or C4B.
e.
C4A and C4B have identical properties.
f.
C4B deficiency is associated with increased susceptibility to systemic lupus
erythematosus.
g.
C4A and C4B are monomorphic.
9–27 Complexes of IgG bound to soluble multivalent antigens can activate the classical
pathway of complement, resulting in the deposition of _____ on the complex, targeting it for
endocytic uptake by cells bearing _____.
a.
C4b; CR2 and Fc receptors
b.
C3b; CR2 and Toll-like receptors
c.
C5-9; CR1 and Fc receptors
d.
C3b; CR1 and Fc receptors
e.
C2a; CR2 and Toll-like receptors.
9–28
a.
b.
c.
d.
A distinguishing feature of FcγRIIB1 compared with FcγRIIA is _____.
its ability to activate cells and induce endocytosis
the existence of ITIMs in its cytoplasmic tails
its inability to bind to IgG1
its expression on NK cells.
9–29
a.
b.
c.
d.
For IgG2 to be effective at stimulating uptake of IgG2-coated bacteria, _____.
an individual must express allotype H131 of FcγRIIA
an individual must express allotype R131 of FcγRIIA
the ITIMs of FcγRIIB2 must be non-functional
complement must be fixed on the surface of the bacterium.
9–30 Describe the ways in which follicular dendritic cells (FDCs) are similar to subcapsular
sinus macrophages.
9–31 Naive B cells search for specific antigen displayed by follicular dendritic cells in primary
follicles. Naive T cells, however, search for specific antigen presented by ______.
a.
dendritic cells
b.
subcapsular sinus macrophages
c.
medullary sinus macrophages
d.
centrocytes
e.
tingible body macrophages.
9–32
a.
b.
c.
d.
e.
Which of the following is consistent with a recently antigen-activated mast cell?
high levels of MHC class II molecules on the cell surface
the absence of prepackaged granules
the absence of IgE on the cell surface
high concentrations of C3b on the cell surface
the induction of antibody-dependent cell-mediated cytotoxicity.
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full file at http://testbankcorner.eu
9–33 Some types of B-cell tumor have been treated with rituximab, an anti-CD20 monoclonal
antibody, which exerts its effect through a mechanism known as ______ involving the
participation of NK cells.
a.
degranulation
b.
neutralization
c.
opsonization
d.
antibody-dependent cell-mediated cytoxicity
e.
receptor-mediated endocytosis.
9–34 Explain why expression of CD40 ligand by TFH cells is important in the boundary area of
primary follicles in secondary lymphoid tissue as it relates to the targeted delivery of secreted
cytokines to the B-cell surface.
9–35 Which of the following is a characteristic of follicular dendritic cells in the primary
follicles of secondary lymphoid tissues? (Select all that apply.)
a.
They are bone marrow derived hematopoietic cells.
b.
They provide a stable depository of intact antigens able to bind to B-cell receptors.
c.
They have a large surface area as a result of forming dendrites.
d.
They internalize immune complexes through CR2 receptor cross-linking.
e.
They produce cytokines that induce B cells to proliferate and become centroblasts.
9–36 A.
What is the main effector function of IgM antibody?
B.
Why is IgM efficient at (i) preventing blood-borne infections and (ii) fixing complement,
but (iii) less efficient than other antibody classes in inducing phagocytosis of immune
complexes?
9–37
A.
Explain how the poly-Ig receptor transports dimeric IgA antibodies across cellular
barriers, and specify the type of cell barrier involved.
B.
What are the final locations of the transported material?
9–38
A.
What are the similarities between the activation of mast cells and NK cells via FcεRI and
FcγRIII, respectively? Be specific.
B.
What are the differences? Again, be specific.
9–39 Describe the course of events that results in the swollen lymph nodes characteristic of
many infections. Use the following terms in your answer: B lymphoblasts, centroblasts,
centrocytes, follicular dendritic cells, germinal center, primary focus, primary follicle, somatic
hypermutation, boundary region, and tingible body macrophages.
9–40
A.
What is meant by the term “passive transfer of immunity,” and how is it achieved? Give
examples.
B.
Give the isotype of the antibodies involved in (i) placental transfer and (ii) transfer into
breast milk, and explain why these antibodies are important.
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full file at http://testbankcorner.eu
C.
Do you think it is possible for a pregnant mother who has an autoimmune disease to
transfer autoreactive antibodies to the developing fetus? Explain your answer.
9–41 Explain the origin of the secretory component and its significance after the release of
dimeric IgA from the apical face of the gut epithelium.
9–42 How does IgE induce the forcible ejection of parasites and toxic substances from the
respiratory and gastrointestinal tracts?
9–43 From an immunological viewpoint, why would it be inadvisable for a mother who has
recently given birth to move with her newborn to a foreign country where there are endemic
diseases not prevalent in her homeland?
9–44
a.
b.
c.
d.
e.
The B-cell co-receptor is composed of
Igα; Igβ; CD19
Igα; Igβ; Lyn tyrosine kinase
CR2 (CD21); CD19; CD81
CD14; CD19; CD81
CD40; MHC class II; CED19.
9–45 C3d and iC3b are breakdown products of _____, which binds to _____ of the B-cell coreceptor.
a.
C3a; CR2
b.
C3b; CR2
c.
C3c; CD81
d.
C3c; CD19
e.
C3b; CD19.
9–46 When bound to CR1, C3b is cleaved by _____, generating pathogen-associated B-cell coreceptor ligands.
a.
factor I
b.
CR2
c.
C3d
d.
CD19
e.
Lyn.
9–47 The Igα-associated tyrosine kinase _____ phosphorylates the cytoplasmic tail of CD19,
which mediates signal transduction in activated B cells.
a.
CD81
b.
Blk
c.
Fyn
d.
Lyn
e.
Syk.
9–48 A B cell’s sensitivity to antigen can be increased 1000–10,0000-fold by
a.
simultaneously ligating the B-cell receptor and co-receptor
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full file at http://testbankcorner.eu
b.
c.
d.
e.
simultaneously ligating the B-cell receptor and Toll-like receptor
ligating the B-cell co-receptor and phosphorylating Ig-α ITAMs
increasing levels of Syk proteins in the vicinity of co-receptor ligation
ligating cytokine receptors on the B-cell surface.
9–49
a.
b.
c.
d.
e.
The process that drives an increase in antibody affinity for antigen is known as _____.
apoptosis
affinity maturation
antibody-dependent cell-mediated cytotoxicity
opsonization
clonal expansion.
9–50
a.
b.
c.
d.
e.
FcRn has which of the following characteristics? (Select all that apply.)
It binds to monomeric IgA in acidified endocytic vesicles.
It transports IgG out of the blood into tissue across the endothelium.
It is similar in structure to an MHC class II molecule.
It protects IgA from degradation by plasma proteases.
Two molecules of FcRn are required to bind to each Fc region.
9–51 The process involving receptor-mediated transport of macromolecules from one side of a
cell to the other is called
a.
phagocytosis
b.
exocytosis
c.
transcytosis
d.
signal transduction
e.
opsonization.
9–52
a.
b.
c.
d.
e.
Of the following, which group of children is the most vulnerable to infection?
babies born at term
babies born prematurely
infants of 3–6 months
infants receiving first vaccination
babies receiving formula and not breast milk.
9–53 _____ occurs as a result of influenza virus binding to oligosaccharide components on
erythrocyte surfaces causing them to clump together.
a.
Passive immunization
b.
Opsonization
c.
Hemagglutination
d.
Neutralization
e.
Complement activation.
9–54 Which of the following are correctly matched? (Select all that apply.)
a.
protein F; fibronectin
b.
neutralization; IgE
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full file at http://testbankcorner.eu
c.
d.
e.
breast milk; IgG
influenza; hemagglutinin
mucosal epithelium; IgA.
9–55
a.
b.
c.
d.
e.
Bacteria use _____ to attach to the surface of cells during colonization.
hemagglutinins
toxins
breakdown products
anti-inflammatory molecules
adhesins.
9–56 Denatured toxin molecules called _____ are used to vaccinate individuals to stimulate the
production of _____.
a.
toxoids; neutralizing IgG antibodies
b.
adhesins; neutralizing antibodies
c.
toxoids; passive immunity
d.
adhesins; complement proteins
e.
toxoids; C-reactive protein.
9–57 Which of the following are characteristics of systemic lupus erythematosus? (Select all
that apply.)
a.
It is an autoimmune disease.
b.
It is associated with a deficiency of C4A.
c.
Increased levels of immune complexes are detected in the blood.
d.
CR1 receptor levels are decreased.
e.
Immune complexes are deposited on the kidney glomeruli, which can lead to kidney
complications.
9–58 The disadvantage of having a longer hinge region in IgG3 compared with the other IgG
subclasses is a reduction in its serum half-life because of its susceptibility to _____.
a.
increased proteolysis by serum proteases
b.
clearance by erythrocytes via FcR binding
c.
immune complex formation and deposition in kidney glomeruli
d.
complement fixation and uptake by cells bearing receptor CR1
e.
opsonization by neutrophils.
9–59 Which of the following antibodies activate the classical pathway of complement? (Select
all that apply.)
a.
IgM
b.
IgG1
c.
IgD
d.
IgG3
e.
IgE.
9–60 The γ chain of the FcγRI receptor is closely related to the _____, which contains _____.
a.
FcRn; MHC class I-like structure
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full file at http://testbankcorner.eu
b.
c.
d.
e.
ζ chain of the T-cell receptor complex; ITAM motifs
γ chain of the FcγRIII receptor; ITIM motifs
γ chain of the FcαRI receptor; ITIM motifs
γ chain of the FcεRI receptor; ITIM motifs.
9–61 Of the Fc receptors for IgG, which one is similar to FcεRI in its ability to bind antibody
in the absence of antigen but does not transduce an activating signal until antigen cross-linking
occurs?
a.
FcγRI
b.
FcγRIIA
c.
FcγRIIB2
d.
FcγRIIB1
e.
FcγRIII.
9–62 Which of the following individuals would be most susceptible to fulminant
meningococcal disease or septic shock when infected with Neisseria meningitidis?
a.
homozygous for allotype H131 of IgG2
b.
heterozygous for allotype H131 of IgG2
c.
homozygous for allotype R131 of IgG2
d.
heterozygous for allotype R131 of IgG2
e.
all of the above would be equally susceptible to infections with Neisseria meningitidis.
9–63 Antibody-dependent cell-mediated cytotoxicity (ADCC) is carried out by _____ after
cross-linking of IgG1 or IgG3 antibodies on _____ receptors.
a.
NK cells; FcγRI
b.
neutrophils; FcγRI
c.
NK cells; FcγRIII
d.
macrophages; FcγRIIB2
e.
mast cells; FcεRI.
9–64 The symptoms of allergy and asthma are induced after cross-linking of IgE antibody on
FcεRI receptors found on the surface of _____. (Select all that apply.)
a.
basophils
b.
eosinophils
c.
macrophages
d.
mast cells
e.
neutrophils.
9–65 The FcαRI receptor binds to _____:antigen complexes and facilitates the phagocytosis of
opsonized antigens.
a.
dimeric IgA
b.
IgM
c.
IgE
d.
IgG
e.
monomeric IgA.
full file at http://testbankcorner.eu
full file at http://testbankcorner.eu
ANSWERS
9–1
c
9–2
b, d
9–3
c
9–4
b
9–5
b
9–6
d
9–7
a, d
9–8
e
9–9
c
9–10 d
9–11 b, e
9–12 b, c, d
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full file at http://testbankcorner.eu
9–13 d
9–14 c
9–15 a—5, b—7, c—4, d—6, e—3, f—1, g—2, h—8
9–16 a
9–17 b
9–18 c
9–19 a—3, b—2, c—4, d—1, e—5
9–20 d
9–21 a
9–22 e
9–23 c, d
9–24 d
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full file at http://testbankcorner.eu
9–25 b
9–26 b, d
9–27 d
9–28 b
9–29 a
9–30 FDCs and subcapsular macrophages use their CR1 and CR2 receptors not for the purpose
of receptor-mediated endocytosis, but rather to bind to antigens tagged with C3d or C3b and to
hold them at the cell surface for extended periods of time. Tethering the antigen in this manner
facilitates screening by naive B cells as they travel through secondary lymphoid tissues.
9–31 a
9–32 b
9–33 d
9–34 CD40 ligand on TFH cells binds to CD40 on B cells, signaling B cells to activate NFκB.
NFκB is a transcription factor that upregulates ICAM-1 expression on B cells, which binds to
LFA-1 on the TFH cell. As a result, cognate interactions between the B cell and TFH cell are
strengthened, and a synapse at the point of contact facilitates the reorientation of the T-cell
cytoskeleton and secretory apparatus of the Golgi. This ensures that T-cell cytokines are released
onto a localized area of the B-cell surface.
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full file at http://testbankcorner.eu
9–35 b, c
9–36
A.
The main effector function of IgM is complement activation; it can also neutralize
pathogens and toxins.
B.
(i) IgM is the first antibody to be produced by plasma cells during a primary
antibody response and is secreted as a pentamer that circulates in the blood. Because of the large
size of pentameric IgM, it does not penetrate effectively into infected tissues and is most
effective against pathogens in the bloodstream. (ii) In the classical pathway of complement
activation, at least two Fc regions are needed to bind C1, the first complement component in the
pathway. A single pentameric molecule of IgM can thus initiate complement activation. In
contrast, two IgG antibodies in close proximity to each other are needed to bind C1. (iii)
Phagocytic cells carry both complement receptors and Fc receptors for IgG (FcγR) and IgA
(FcαR), but there are no Fc receptors for IgM. Thus, immune complexes of IgM and antigen
alone cannot be taken up by macrophages through Fc receptor-mediated endocytosis. An
IgM:antigen:C3b complex can be phagocytosed by a macrophage after binding to complement
receptors, but this is not as efficient as having both complement receptors and Fc receptors
cooperating in inducing phagocytosis.
9–37
A.
Dimeric IgA is made in mucosa-associated lymphoid tissue (MALT) and is
transported across the barrier of the mucosal epithelium. First, dimeric IgA binds to the poly-Ig
receptor on the basolateral surface of an epithelial cell, followed by uptake through receptormediated endocytosis into an endocytic vesicle. On reaching the opposite face of the cell, the
apical surface, the vesicle fuses with the membrane. Here the poly-Ig receptor is cleaved
proteolytically between the membrane-anchoring and the IgA-binding regions, thus releasing
IgA into the mucous layer on the surface of the epithelium. Dimeric IgA remains attached to a
small piece of the poly-Ig receptor, called the secretory component, which holds the IgA at the
epithelial surface through interactions with molecules in the mucus. The rest of the poly-Ig
receptor is degraded and serves no further purpose.
B.
Dimeric IgA is released into the lumen of the gastrointestinal, urogenital, and
respiratory tracts, onto the surface of the eyes, into the nose and throat, and into breast milk
(which is the route by which newborn babies receive protective maternal IgA).
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full file at http://testbankcorner.eu
9–38
A.
Similarities: (1) Activation of both mast cells and NK cells occurs only when their
Fc receptors are bound to antigen:antibody complexes. (2) When cross-linking occurs, both mast
cells and NK cells release the contents of granules through exocytosis, which involves the fusion
of vesicles containing preformed proteins with the cell membrane.
B.
Differences: (1) Mast cells bind IgE, whereas NK cells bind IgG. (2) Exocytosis
of granules from mast cells occurs at random around the cell membrane. Exocytosis of granules
from NK cells is highly polarized, focusing only on the target cell to minimize damage to
neighboring cells. (3) IgE binds to FcεRI with high affinity in the absence of antigen; mast cells
become activated when antigen becomes available and binds to the receptor-bound IgE. NK cells
bind IgG with low affinity, and bind IgG effectively only when it is already bound to multivalent
antigen. (4) Activated mast cells release inflammatory mediators (histamine and serotonin) that
affect other cells, for example endothelium, causing increased vascular permeability and
vasodilation. Activated NK cells release apoptosis-inducing compounds (perforin and
granzyme/fragmentin) that kill target cells directly. (5) Antibody-dependent cell-mediated
cytotoxicity (ADCC) carried out by NK cells could be induced in newborn infants by maternal
IgG acquired transplacentally. IgE cannot be transferred across the placenta, and so newborn
babies cannot activate mast cells via maternal IgE.
9–39 B lymphoblasts that have bound specific antigen and encountered their cognate T cells in
the boundary regions between primary follicles and the T-cell area of a lymph node are activated
and start to proliferate, forming a primary focus. The B cells move from the primary foci into
primary follicles, which are primarily B-cell areas, where they become centroblasts—large,
metabolically active, dividing cells. As centroblasts accumulate and proliferate, the primary
follicle enlarges and changes morphologically into a germinal center. Centroblasts undergo
somatic hypermutation while dividing in the germinal center, producing centrocytes with
mutated surface immunoglobulin. Only cells with mutated surface immunoglobulin that can take
up antigen efficiently through receptor-mediated endocytosis and present it to helper T cells
(TFH) will be selected to differentiate into plasma cells or memory cells. Antigen will be
encountered at the surface of follicular dendritic cells as an immune complex. If B cells do not
encounter their specific antigen, they will undergo apoptosis and then be ingested and cleared by
tingible body macrophages. This process takes around 7 days after an infection begins, and the
increase in cell numbers due to lymphocyte proliferation accounts for the swollen lymph nodes.
9–40
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A.
Passive transfer of immunity refers to the process of transferring preformed
immunity from an immune subject to a nonimmune subject. This can be achieved by transferring
whole serum (antiserum), purified antibody, monoclonal antibody, or intact effector or memory
lymphocytes (adoptive transfer).
B.
(i) IgG antibodies transported transplacentally provide passive protection in the
bloodstream and extracellular spaces of tissues until the baby can begin making its own
antibodies, after which time maternal IgG levels decrease. (ii) IgA is transferred into the infant’s
gastrointestinal tract in breast milk and protects the gastrointestinal epithelia from colonization
and invasion by ingested microorganisms.
C.
It is possible for autoreactive antibodies to be transferred passively to a fetus via
the placenta if the isotype is IgG. Any reaction will persist only for as long as the antibodies are
present.
9–41 During transcytosis the poly-Ig receptor is cleaved by a protease, leaving a small piece of
the original receptor, called the secretory component, still bound to the J chain via disulfide
bonds. Once dimeric IgA is released at the apical face, the carbohydrate moieties of the secretory
component anchor the antibody to mucins of the mucus, enabling the antibodies to bind
subsequently to microbes in the mucus and inhibit the ability of microbes to bind to and invade
the mucosal epithelium of the gut. Instead, the microbe is expelled from the body via mucosal
secretions in the feces.
9–42 When IgE binds to antigen, leading to cross-linking of FcεRI on mast cells in connective
and mucosal tissues, the mast cells rapidly release chemicals that activate smooth muscle to
contract. Muscle activity leads to vomiting and diarrhea in the gastrointestinal tract, and sneezing
and coughing in the respiratory tract, helping to expel the offending pathogen or toxic material.
9–43 Newborn infants are afforded passive immunity to the pathogens in their environment
through IgG and dimeric IgA. IgG is transferred transplacentally, and dimeric IgA is acquired
through breast milk. If an endemic infection develops in the newborn infant, the IgG antibodies
in the infant’s bloodstream may not have the appropriate specificity for the foreign antigens
because the mother would not have encountered these antigens previously in their homeland, and
therefore the newborn infant would not have acquired them passively during fetal development.
Furthermore, without maternal IgG, infants are particularly susceptible to infection for the first
6 months of their life, when their immune systems are unable to produce significant levels of
IgG. In addition, infections that breach mucosal surfaces may be more likely to develop during
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this time because dimeric IgA against such a pathogen will not be formed in the breast milk until
about a week after the mother has been exposed to the same pathogen.
9–44 c
9–45 b
9–46 a
9–47 d
9–48 a
9–49 b
9–50 b, e
9–51 c
9–52 b
9–53 c
9–54 a, d, e
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9–55 e
9–56 a
9–57 a, b, c, e
9–58 a
9–59 a, b, d
9–60 b
9–61 a
9–62 c
9–63 c
9–64 a, b, d
9–65 e
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