Test Bank for Basic Immunology, 3rd Edition: Abul K.

Abbas

Test Bank for Basic Immunology, 3rd Edition: Abul

K. Abbas

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Chapter 06: Effector Mechanisms of T Cell–Mediated Immunity

Test Bank

MULTIPLE CHOICE

1. Which of the following statements about cell-mediated immunity (CMI) is NOT true?
A. Deficiencies in CMI result in susceptibility to infections by viruses and
intracellular bacteria.
B. CMI can be adoptively transferred by injecting serum from one individual to
another.
C. Delayed-type hypersensitivity (DTH) is not a protective response against
intracellular bacteria such as Mycobacterium tuberculosis.
D. The principal form of CMI that protects against viral infections is mediated by
CD8+ cytolytic T lymphocytes.
E. Phagocytes are essential in the effector phase of CMI responses to bacteria such
as Listeria monocytogenes.

ANS: B
The original definition of cell-mediated immunity (CMI), which is still valid, is
protection against infection that can be transferred by T cells but not by serum. Serum is
a cell-free fraction of blood that includes antibodies, and therefore serum transfer can
provide passive humoral immunity. CMI is required for protection against microbes that
can reside within cells and therefore are inaccessible to antibodies. These organisms
include microbes that are phagocytosed and viruses that replicate in the cytoplasm.
Immunodeficiency states in which CMI is impaired (e.g., AIDS) result in infections by
viruses and intracellular bacteria or fungi. Delayed-type hypersensitivity (DTH), like all
hypersensitivity reactions, causes tissue damage and disease, but not protection. It is true
that DTH reactions involve the same cells and molecules as does CMI.

2. The induction phase of a cell-mediated immune response includes which of the

following events?
A. CD4+ T cell secretion of interferon- leading to macrophage activation
B. CD8+ T cell lysis of a virally infected cell
C. Clonal expansion of CD8+ T cells within a lymph node
D. Migration of CD4+ effector T cells from blood vessels into a tissue site of
infection
E. Migration of a naive CD4+ T cell from the thymic medulla into the circulation

ANS: C
The induction phase of cell-mediated immune responses occurs in lymphoid tissues and
includes antigen presentation to naive T cells, leading to clonal expansion and
differentiation of those T cells into effector cells. Migration into infection sites and
interferon- secretion by CD4+ helper T cells, as well as target cell killing by CD8+CTL,
are part of the effector phases of cell-mediated immune responses. Naive T cell migration

Copyright © 2014, 2011, 2009, 2006, 2004, 2001 by Saunders, an imprint of Elsevier Inc.
Test Bank 6-2

out of the thymus is the last step in T cell maturation and occurs regardless of the
presence of antigen.

3. Which of the following comparisons between TH1 and TH2 cells is true?
A. TH1 cells produce interleukin (IL)-1 but not IL-2, and TH2 cells produce IL-2 but
not IL-1.
B. TH1 cells are class I major histocompatibility complex (MHC) restricted, and
TH2 cells are class II MHC restricted.
C. The chemokine receptors CXCR3 and CCR5 are more highly expressed on TH2
cells than on TH1 cells.
D. TH2 cells are more likely to bind to E-selectin and P-selectin on endothelial cells
than are TH1 cells.
E. TH1 cells produce interferon (IFN)- but not IL-4, and TH2 cells produce IL-4 but
not IFN-

ANS: E
The signature cytokines of TH1 and TH2 cells are interferon- and interleukin (IL)-4,
respectively. IL-5 and IL-13 are also very specific for TH2 cells. IL-1 is not typically
produced by helper T cells of either subset. IL-2 is produced by naive T cells and TH1
cells. Both TH1 and TH2 cells are CD4+ helper T cells, and therefore are both restricted
to recognizing peptide antigens bound to class II MHC molecules. The trafficking
patterns of TH1 and TH2 cells differ, and this is related to differences in the expression
of adhesion molecules and chemokine receptors. TH1 cells express abundant functional
ligands for E-selectin and P-selectin and the chemokine receptors CXCR3 and CCR5,
which bind to various chemokines found at sites of active innate immune responses. TH2
cells bind poorly to endothelial selectins and express less CXCR3 and CCR5.

4. Differentiation of TH2 cells from naive precursor cells is dependent on which of the
following?
A. Toll-like receptor (TLR) ligands
B. T-bet
C. Interleukin-12
D. GATA-3
E. Interferon-

ANS: D
GATA-3 is a transcription factor that is expressed during differentiation and is required
for TH2 differentiation. T-bet is a protein that regulates genetic changes required for TH1
differentiation. In general, innate immune responses, many of which are stimulated
microbial products binding Toll-like receptors (TLRs) on antigen-presenting cells
(APCs), promote TH1 differentiation. In part, the positive influence of innate immune
responses on TH1 differentiation is mediated by cytokines secreted by activated APCs,
including interleukin-12 and type I interferons (IFN- and IFN-).

Copyright © 2014, 2011, 2009, 2006, 2004, 2001 by Saunders, an imprint of Elsevier Inc.
Test Bank 6-3

5. The mechanisms by which TH1 cells protect against microbes include all of the
following EXCEPT:
A. Secretion of interferon (IFN)- which activates microbicidal functions of
macrophages
B. Expression of CD40 ligand, which binds to CD40 on macrophages and activates
them
C. Secretion of IFN-, which promotes B cell production of opsonizing antibodies
D. Secretion of lymphotoxin and tumor necrosis factor, which enhance neutrophil
killing of ingested microbes
E. Release of granzyme B, which stimulates apoptosis of bacteria

ANS: E
Granzyme B, a product of CD8+ cytolytic T lymphocytes, promotes death of infected
host cells, but not of extracellular microbes. The principal function of TH1 cells is to
enhance phagocyte defense against intracellular infections. Interferon (IFN)- and CD40
ligand, produced by TH1 cells, enhance killing of microbes ingested by macrophages, in
part by stimulating the production of inducible nitric oxide synthase and phagocyte
oxidase. IFN-, produced by TH1 cells, is an isotype switch factor, promoting the
production of IgG subtypes that bind to Fc receptors on phagocytes and fix complement.
Therefore, these opsonizing IgG subtypes facilitate the phagocytosis of the microbes to
which they bind. TH1 cells also secrete tumor necrosis factor and lymphotoxin, two
cytokines that can activate neutrophil killing of internalized microbes.

6. Activated macrophages perform all of the following functions EXCEPT:

A. Inhibition of fibroblast proliferation and angiogenesis within damaged tissues
B. Production of lysosomal enzymes and reactive oxygen species that kill
phagocytosed microbes
C. Presentation of antigen to helper T cells
D. Secretion of inflammatory cytokines such as tumor necrosis factor and
interleukin-1
E. Production of nitric oxide, which helps kill microorganisms

ANS: A
Activated macrophages, through the secretion of growth factors, promote fibroblast
proliferation and angiogenesis in an effort to repair damaged tissues.

7. Which of the following molecules is NOT important in the interaction between a

cytolytic T lymphocyte and a target cell?
A. B7-1
B. ICAM-1
C. LFA-1
D. T cell receptor
E. Class I MHC

ANS: A
Although naive CD8+ T cells require second signals, such as B7 costimulation, in order
to differentiate into effector cytolytic T lymphocyte (CTL), once differentiated, the CTL

Copyright © 2014, 2011, 2009, 2006, 2004, 2001 by Saunders, an imprint of Elsevier Inc.
Test Bank 6-4

can kill a target cell that does not express costimulatory molecules. The CTL only
requires one signal for killing of the target cell, which depends on the T cell receptor
binding to a peptide-class I MHC complex on the surface of the target cell. Tight
adhesion between the CTL and target cell is also required, and this is often mediated by T
cell integrin LFA-1 binding to target cell ICAM-1.

8. Which pair of molecules is a component of cytolytic T lymphocyte (CTL) granules

and is important in the mechanism of CTL killing of target cells?
A. Perforin and Fas ligand
B. P-selectin and tumor necrosis factor
C. Major basic protein and granzyme B
D. C9 and interferon-
E. Perforin and granzyme B

ANS: E
Perforin and granzyme B are the cytolytic T lymphocyte (CTL) granule constituents of
most importance in killing of target cells. CTL granules are emptied by exocytosis into
the intercellular space between the CTL and target cell. Here perforin polymerizes to
form pore-like structures that insert into the target cell plasma membrane and/or in the
membranes of endocytic vesicles in the target cell. Granzyme B is a proteolytic enzyme
that cleaves substrates in the cytoplasm of the target cell, leading to a cascade of enzyme
activation that ends in apoptosis. Granzyme B enters the target cell either through
perforin pores or by receptor-mediated endocytosis. FasL is expressed on the surface of
the CTL, not in granules. FasL binding to Fas on target cells may induce apoptosis of the
target cells by a caspase-dependent pathway, but this is a minor mechanism of CTL
killing relative to perforin- and granzyme B–dependent mechanisms. P-selectin is an
endothelial adhesion molecule stored in cytoplasmic granules, and MBP is a cationic
protein found in eosinophil granules. Although perforin is homologous to the
complement protein C9, C9 is not present in CTL granules. CTLs do produce interferon-
, but they do not store this cytokine in granules.

9. Which of the following mechanisms does NOT contribute to the generation of a

cytolytic T lymphocyte (CTL) response to a viral infection?
A. Dendritic cells phagocytose infected cells or viral particles and present them to
naive CD8+ T cells via the class I MHC pathway.
B. Dendritic cells are infected with the virus and present viral peptides to naive
CD8+ T cells via the class I MHC pathway.
C. CTLs are directly activated by CD40L expressed on activated helper T cells
through CD40.
D. Helper T cells secrete cytokines, such as interleukin-2, that promote the
proliferation and differentiation of CD8+ T cells.
E. Helper T cells activate infected antigen-presenting cells (APCs) via the CD40
ligand-CD40 pathway, and the activated APCs present viral peptides to naive CD8+
T cells via the class I MHC pathway.

ANS: C

Copyright © 2014, 2011, 2009, 2006, 2004, 2001 by Saunders, an imprint of Elsevier Inc.
Test Bank for Basic Immunology, 3rd Edition: Abul K. Abbas

Test Bank 6-5

T cells do not express CD40, and they do not respond directly to CD40 ligand. There is
clear evidence that CD8+ cytolytic T lymphocyte (CTL) responses to viral infections
require professional antigen-presenting cells (APCs) as well as CD4+ helper T cells. How
this works is complicated; all viruses do not infect professional APCs, and helper T cells
are class II MHC restricted whereas CD8+ CTL precursors are class I MHC restricted.
Several mechanisms have been shown to contribute to naive CD8+ T cell activation in
experimental systems. One mechanism is cross presentation of viral peptides by
professional APCs that were not infected but acquired the viral antigens from other cells.
Infected APCs may present viral peptides to CD4+ T cells, stimulating a helper T cell
response, which then, via secreted cytokines, helps activate CD8+ T cells. Helper T cells
may also enhance APC function of infected cells via CD40-CD40 ligand interactions.

10. A 23-year-old man who was recently infected by the HIV virus volunteered for
investigative studies of his immune response to the virus. Investigators identified
cytolytic T lymphocytes (CTLs) in the patient’s blood that recognized a particular peptide
derived from a protein encoded by the HIV gag gene. Six months later, viral isolates
from the patient showed point mutations in the gag gene sequence encoding that peptide.
Which of the following statements about the HIV gag mutations is most likely to be
correct?
A. The patient’s CTL response to the virus provided selective pressure for the
emergence of virus carrying the mutation.
B. The CTL that recognized the original gag-encoded peptide will still be able to
recognize the mutated Gag peptide.
C. The CTLs specific for the original Gag peptide were incapable of killing HIV-
infected cells.
D. The gag mutation will enhance the ability of natural killer cells to recognize and
kill HIV infected cells.
E. The gag mutations have more relevance to the viral evasion of the antibody
response rather than the CTL response.

ANS: A
Cytolytic T lymphocytes (CTLs) are highly specific for short peptide epitopes of viral
proteins bound to self-MHC molecules. Random mutations in the viral genome that alter
these peptide sequences will lead to escape from CTL detection. Therefore, CTLs do
provide a selective pressure for such mutations. Given these selective pressures, it is most
likely that the mutations that are found in the virus that has survived in the patient are no
longer recognized by the CTL. Because only one or two amino acid residues of a viral
peptide will contact a particular TCR, point mutations that ablate T cell recognition are
likely to occur. The emergence of escape variants with mutated peptides implies that the
CTLs that recognized the original peptide were capable of killing the infected cells, but
mutations arose before all infected cells were killed. Natural killer cells recognize
alterations in self class I MHC expression but do not recognize specific viral peptide
sequences. Although antibodies may be produced specific for distinct epitopes of the
same proteins that elicit CTL responses, the information given about changes in a T cell
epitope implicate the relevance of the CTL response.

Copyright © 2014, 2011, 2009, 2006, 2004, 2001 by Saunders, an imprint of Elsevier Inc.

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