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Janeways Immunobiology 9th Edition by Kenneth Murphy; Casey Weaver |
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Test bank for Janeways Immunobiology 9th Edition byKenneth Murphy; Casey Weaver | 9780815345053 | Chapter
1-16 | All Chapters with Answers and Rationals
9.1 Multiple choice: Secondary lymphoid organs, such as the lymph nodes, spleen, and mucosa-
associated lymphoid tissues, each have distinct features that are important for
their role in initiating immune responses focused on different anatomical compartments (i.e., the
peripheral tissues, the blood, or the gastrointestinal tract, respectively). Yet these organs share some
overall structural features, such as distinct T-cell and B-cell zones. One major difference between
these organs is:
A. The presence versus the absence of macrophages and dendritic cells
B. Their function in bringing rare naive lymphocytes into contact with their specific antigen
C. The ability of lymphocytes to enter the organ from the blood
D. The mechanism by which antigens or pathogens enter the organ
E. The ability of naïve T cells to be activated and proliferate in the organ - ANSWER: D. The mechanism
by which antigens or pathogens enter the organ
9.2 Multiple choice: The TNF family of cytokines and their receptors are critical for the development
of secondary lymphoid organs, such as the lymph nodes and Peyer's
patches. As a consequence, knockout mice lacking expression of LT-beta fail to develop most of these
structures. Reconstitution of irradiated LT-beta-deficient mice with bone marrow stem cells from
wild-type mice (e.g., LT-beta-sufficient) would:
A. Restore all missing lymphoid structures in the recipient mice
B. Restore the missing lymphoid structures but not the missing follicular dendritic cells in the recipient
mice
C. Restore the missing follicular dendritic cells but not the missing lymphoid structures in the recipient
mice
D. Have no effect on any lymphoid structures in the recipient mice
E. Only restore the proper organization of B cell follicles in the recipient mice - ANSWER: C. Restore
the missing follicular dendritic cells but not the missing lymphoid structures in the recipient mice
9.3 Multiple choice: An immunodeficient mouse strain is identified, that has a single gene defect
causing its disease. Mice with this defect have greatly impaired responses to
protein antigens following subcutaneous immunization and also exhibit severely delays in the kinetics
of their antibody responses. Analysis of their lymph nodes revealed
profound alterations in the normal architecture, with a lack of organization of distinct T-cell and B-cell
zones. A likely candidate for the defect in these mice is:
A. The chemokine receptor CCR7, which recruits B cells, T cells, and dendritic cells to lymph nodes.
B. The TNF family member LT-, which is made by Lti cells.
C. The chemokine receptor CXCR5 that recruits B cells to the lymph node follicles.
D. Prox1, the transcription factor required for the development of lymphatic vessels.
E. TNF-, which is required for the development of FDCs. - ANSWER: A. The chemokine receptor CCR7,
which recruits B cells, T cells, and dendritic cells to lymph nodes.
9.4 Multiple choice: Strep throat is commonly caused by group A Streptococcus bacteria. A common
symptom of strep throat is the presence of swollen lymph nodes in the neck. This symptom usually
peaks about 2-4 days after the onset of the infection, and is due to:
,A. Damage to the pharyngeal epithelium by the bacteria
B. Release of bacterial PAMPs leading to inflammatory cytokine production
C. Trapping and activation of antigen-specific lymphocytes in the lymph nodes of the neck
D. Recruitment of neutrophils to the lymph nodes of the neck
E. Recruitment of circulating macrophages to the lymph nodes of the neck - ANSWER: C. Trapping and
activation of antigen-specific lymphocytes in the lymph nodes of the neck
9.7 Multiple choice: When T cells are activated by recognizing peptide:MHC complexes on dendritic
cells in the lymph node, they up-regulate the receptor CD69. For T cells
expressing a given T-cell receptor, the initial strength of the T-cell receptor signal can be modulated
by varying the number of peptide:MHC complexes on the dendritic cells, or by varying the affinity
with which the T cell-receptor binds to the peptide:MHC complexes. As a result, T cells stimulated
with stronger T-cell receptor signals will
maintain high expression of CD69 for one or two days longer that if those same T cells were
stimulated with weaker T-cell receptor signals. Therefore, T cells stimulated with weaker T-cell
receptor signals are likely to:
A. Die by apoptosis
B. Undergo more rounds of proliferation that T cells stimulated with stronger T-cell receptor signals
C. Migrate to the B-cell zones of the lymph node
D. Have reduced effect - ANSWER: E. Egress from the lymph node 1-2 days earlier than T cells
stimulated with stronger T-cell receptor signals
9.8 True/False: Unlike innate immune responses, adaptive immune responses are initiated in
secondary lymphoid organs. However, the innate immune response to an infection in a tissue has a
pivotal role in inducing T-cell responses in the nearest lymph node by activating tissue dendritic cells
and inducing their migration to the lymph node. - ANSWER: True
9.10 Multiple choice: A mouse is infected with staphylococcal bacteria through a laceration
in the skin of its paw. Dendritic cells are isolated from the tissue at the site of infection, and are
incubated together with naïve staphylococcal-specific CD4 T cells. Seventy-two hours later, the
proliferation of the CD4 T cells is measured as a readout for T cell activation. Surprisingly, the T cell
response is quite poor compared to the response
observed when the same T cells are mixed with a comparable number of dendritic cells isolated from
the draining lymph node of the infected mouse. A comparison of the dendritic cells isolated from the
two different sites would reveal:
A. Much higher levels of MHC and B7 molecules on the lymph node dendritic cells than those from
the infected tissue
B. Much higher expression of all TLRs in the lymph node dendritic cells than those from the infected
tissue
C. An increased number of - ANSWER: A. Much higher levels of MHC and B7 molecules on the lymph
node dendritic cells than those from the infected tissue
9.11 Multiple choice: Many virus infections induce robust production of type I interferons, IFN-alpha
and IFN-beta. One example is the herpes simplex virus-1 (HSV-2), one of the most common sexually
transmitted diseases in the US. Experiments that investigated the immune response to HSV-2 using a
mouse model demonstrated essential roles for the
DNA sensing Toll-like receptor, TLR9, and its downstream signaling adapter, MyD88, in the production
of type I interferons following HSV-2 immunization. The type I interferon response to HSV-2 would be
restored in Tlr9-/- mice by transferring into these mice wildtype:
A. Macrophages
B. Conventional dendritic cells
C. Mast cells
D. Plasmacytoid dendritic cells
E. Neutrophils - ANSWER: D. Plasmacytoid dendritic cells
, 9.12 Multiple choice: When macrophages in the lung are infected with an intracellular bacterium,
such as Mycobacterium tuberculosis, they are activated by the interactions of their pattern
recognition receptors with the microbe. These activated macrophages will
then:
A. Migrate to the marginal sinus of the draining lymph node to activate naive CD4 T cells
B. Increase their phagocytic properties to scavenge dead and dying neighboring cells
C. Migrate to the liver where they will remove dying cells from the blood
D. Migrate to the red pulp of the spleen where they will remove immune complexes from the
circulation
E. Up-regulate MHC class II and B7 molecules to amplify CD4 T cell responses in the lung - ANSWER: E.
Up-regulate MHC class II and B7 molecules to amplify CD4 T cell responses in the lung
9.13 Multiple choice: To generate a vaccine to pertussis toxin, a heat-killed preparation of Bordetella
pertussis (the bacteria that produce pertussis toxin) is mixed with a purified
preparation of the inactivated toxin protein. The mixture is then injected subcutaneously into mice. In
an effort to enhance the antibody response to the toxin, a group of test mice is depleted of all their
dendritic cells immediately prior to immunization. However, instead of enhancing the antibody
response, the dendritic cell depletion nearly eliminated the anti-toxin antibody response because:
A. All of the toxin-specific B cells underwent apoptosis in the absence of dendritic cells.
B. The heat-killed Bordetella pertussis could not be ingested by macrophages in the mice.
C. Dendritic cells are needed to activate naive CD4 T cells, which can then help the B cells produce
anti-toxin antibody.
D. The macrophages in the mice did not exp - ANSWER: C. Dendritic cells are needed to activate naive
CD4 T cells, which can then help the B cells produce anti-toxin antibody.
9.14 True/False: Naive T cells scan the dendritic cells in the cortical region of the lymph node as they
migrate. The initial encounter of T cells with dendritic cells is mediated by
interactions between the T-cell receptor and the peptide:MHC complexes on the dendritic cell. -
ANSWER: False
9.15 Multiple choice: Purified naive T cells isolated from a T-cell receptor transgenic mouse represent
a homogeneous population of cells with specificity for a single known
peptide:MHC complex. This specific peptide:MHC complex can be purified and formed into
multivalent complexes, such as peptide:MHC tetramers. When the naive T cells are
stimulated with their 'antigen' in the form of these peptide:MHC tetramers, the T cells show
activation responses, including the up-regulation of genes that are induced within several hours after
T-cell receptor stimulation. However, these activated T cells fail to
undergo robust proliferation, and the majority of cells die after 3-4 days in culture. T cell proliferation
and survival could be greatly augmented by addition of:
A. Anti-inflammatory cytokines
B. Toll-like receptor ligands
C. Antibodies to the T-cell receptor
D. B7 ligands for CD28
E. The integrin LFA-1 - ANSWER: D. B7 ligands for CD28
9.17 Multiple choice: While CD28 co-stimulation is important for the initial activation of naive T cells,
other co-stimulatory molecules function at later stages of the T cell response.
Several of these other co-stimulatory molecules are members of the TNF-receptor family, and
function by activating the transcription factor, NFB. Therefore, stimulation of these co-stimulatory
TNF-receptors on activated T cells is likely to:
A. Induce programmed cell death in the T cell
B. Enhance T cell survival
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