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Biol 430
Question Bank
1. What are the four characteristics
of the adaptive immune system?
Overview
For each characteristic, explain how the innate
immune system is different.
1. _______________________:
2. _______________________:
3. _______________________:
4. _______________________:
2. Mark each space as True (T) or False (F):
Immune system
Uses
receptors
Relatively fast
response
Pathogen-specific
response
Involves
Macrophages
Innate
Acquired
3. Complete the following table:
Cell
Type
Type of
coreceptor it
carries
Type of
MHC it
interacts with
Cells that present AGs to this type
of lymphocyte
TH
TC
4. Activation of a B-cell and its development into a plasma cell requires two signals. Explain.
Biol 430
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5. Following an infection, memory B-cells are produced. Although these memory cells are relatively
low in number, they can provide immunity to a future infection by the same pathogen.
A. How can a small number of memory cells provide immunity?
B. These memory cells can provide immunity toward the same pathogen but not others;
why?
6. According to the clonal selection theory: (be clear and concise)
1) Why do only certain types of B-cells proliferate in response to a particular antigen/
2) What happens to a B-cell after it begins to proliferate?
3) Why does this process lead to future immunity to pathogen?
7. Match the following terms with their proper descriptions.
Immune component
Description
a. ___ B-cell
1. can activate either Tc or TH cells
b. ___ TH cell
2. is the effector Tc cell
c. ___ Effector
3. cell providing hormonal stimulation to both B- and T-cells
d. ___ Toll-like receptor
4. example of a T-cell coreceptor
e. ___ CTL
5. proteins produced by plasma cells
f. ___ Tc cell
6. activated cell that mediates an immune response
g. ___ Plasma cell
7. naïve cell of the humoral arm of the adaptive system
h. ___ MHC
8. molecule upon which peptide antigens are displayed to T-cells
i. ___ BCR
9. effector cells of the humoral response
j. ___ CD8
10. A broadly specific receptor of the innate immune system
k. ___ Cytokine
11. receptor on naïve B-cells
l. ___ Professional APC
12. also known as a CD8 cell
m. ___ Antibodies
13. hormonal molecules mediating immune cell communication
n. ___ Naïve cell
14. an immune cell yet to encounter an appropriate antigen
Biol 430
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8. Suppose that you were exposed on your skin to a pathogenic strain of Staphylococcus aureus, a
common but potentially serious extracellular pathogen. After about three days you had developed a
severe skin infection, which began to subside on its own within a week.
A. Describe the innate defenses that the pathogen overcame during the first three days.
B. Which arm of the acquired immune response was most important for directly attacking
this pathogen? What role would the other arm need to play?
C. Describe the steps that lead to activation of the acquired response that eventually
controlled the defenses.
9. Would each of the following types of mutations most directly affect functioning of the (I) innate
or the (A) acquired immune response? Briefly explain your answers
A. Inactivation of the TLR-4 toll-like receptor ___:
B. Immune deficiency in the ability to produce B-cells ___:
C. A mutation in the pathway needed to form a functional TCR ___:
D. An inability of macrophages to display peptides on MHC-II ___:
Biol 430
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10. Identify the components of the interacting T-cell and antigen presenting cell diagrammed below.
A. __________________
B. __________________
C. __________________
D. __________________
11. A patient is subject to recurrent infections by intracellular pathogens (such as viruses) but with
normal resistance to extracellular pathogens (most bacteria). Explain why each of the following
statements is either (C) correct, (PC) possibly correct or (I) incorrect:
A. The deficiency affects the cell-mediated arm of the acquired immune system. ___
B. The deficiency affects the humoral arm of the acquired immune system. ___
C. The deficiency lies specifically within the function of antigen-presenting cells. ___
D. The patient is not producing a sufficiently large enough diversity of Tc cells. ___
12. As we will learn in upcoming chapters, of all the B-and T-cells that begin development, over
90% undergo apoptosis and die before being released to the body. If the body were less
discriminating, more of these cells, with a broader range of antigen recognition, could be produced
to yield better protection against pathogens. Explain why this might also have undesirable
consequences for the body.
Biol 430
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13. The origin of memory cells during immune activation has been of great interest. Recently it was
suggested (Chang, et al. 2007. Science 315:1687-1691) that during the first cell division of a T-cell
upon activation the daughter cells become imprinted to become either effector or memory T-cells.
Activation of a T-cell occurs as it interacts with a
professional antigen presenting cell, such as a dendritic
cell. The contact surface between the two cells, called the
“immune synapse” is where cell surface proteins interact
and toward which many cytoplasmic proteins are recruited.
The result is that, upon cell division, various proteins (cell
determinants) become asymmetrically distributed between
the two daughter cells (proximal and distal cells are located
near or away from the synapse, respectively). It is
proposed that these proteins determine whether the cell
goes on to become an effector or memory cell.
A. What types of surface molecules on the antigen presenting cell and the T-cell must interact
within the immune synapse?
B. What is the difference between a naïve Tc cell and its effector cell? What is the name for
an effector Tc cell?
C. How is the property of a memory cell different from that of an effector cell?
The authors performed several analyses of the proximal and distal daughter cells to see if they
showed characteristics of memory or effectors Tc cells. In one experiment, they looked for the
presence in the cells of the “cytokine IL-7Rα
receptor”, a marker of early memory cell
precursors, by quantifying its mRNA; the results
are shown in Graph A. In another experiment,
they looked at the ability of the proximal and
distal cells to combat an infection. Either
proximal or distal cells were transferred to
recipient host mice, which were then infected with
an intracellular pathogen (Listeria
monocytogenes) immediately (acute) or after 30
days (delayed). Four days after infecting the
mice, the relative numbers of bacteria (‘bacterial
burden’) were counted. The results of this experiment are shown in Graph B.
(continued on next page)
Biol 430
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D. What is a cytokine and a cytokine receptor?
E. In the second experiment, infecting the mice acutely or after a 30-day delay helps to
distinguish between effector and memory T-cells. Explain.
F. An intracellular pathogen is used to infect the mice. Why? Why not an extracellular
pathogen?
G. Both cell types are equally effective in defending against the acute infection, but the
proximal cells are less effective for a delayed infection. Why?
H. Which of the cells displays the characteristics of memory cells? Do results of both
experiments agree? Explain.
14. Va Heijst et al (Science 325:1265; 2009) investigated whether the strength of the cell-mediated
immune response is due to either the 1) number of different types of T-cells activated or 2) the
amount of clonal expansion that occurs. To do so, they generated a large number of Tc cells with a
TCR specific for hen ovalbumin (OVA) each of which also contained a distinctive genetic sequence
(“barcode”). The barcode allowed the researchers to track how many antigen-specific T-cells
respond to an infection and the total number of these cells that were produced after clonal expansion
(all the progeny cells also will contain the same barcode).
Mice were preloaded with 1000 barcoded T-cells (although not all of these cells had a different bar
code) and then injected with different amounts on Listeria monocytogens (Lm) genetically
engineered to express a specific OVA epitope. At the peak of the immune response (8 days later),
the total number of barcoded T-cells was determined (Figure A). Then for mice showing different
levels of immune response, they determined the number of different barcodes among the activated
T-cells (Figure B).
Biol 430
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A. Noting that the scales on the graphs are logarithmic, what is the approximate highest and
lowest dosage of Lm used?
B. How can you tell how strongly the T-cells responded (“clonally expanded”)? By how much
did the total number of barcoded T-cells in the spleens increase from the highest to the lowest
Lm dosage?
C. Noting that the injected T-cells were genetically barcoded, how can you determine how many
of these cells responded infection with Lm-OVA? Did the number of T-cells that responded
change with the Lm dosage?
D. Do these results indicate that it was the number of T-cells that were activated or the extent of
clonal expansion that determined the strength of the immune response? Explain.
The researchers also examined how effectively T-cells were recruited
during an immune response. For this experiment, 5000 OVA-specific
T-cells tagged with a marker that disappears when the cells become
activated were injected into mice (we’ll skip over the details). The mice
were then left uninfected, infected with wild-type Lm. or infected with
Lm expressing OVA. Eight days later the number of unactivated OVAspecific T-cells were measured, and the results are shown in Figure C.
E. Why did the researcher leave some mice uninfected and infect
some with wild-type Lm?
F. What approximate percentage of the OVA-specific T-cells were recruited into the immune
response? Explain.
The authors also noted:
“The observed efficiency of recruitment also indicates that the process through which naïve T cells scan antigenpresenting dendritic cells (DCs) must be sufficiently robust to allow the vast majority of antigen-specific Tcells to
encounter a DC carrying cognate antigen within the first 72 hours of infection. Assuming that naïve antigen-specific
CD8+ T-cells are present at a frequency of ~1:100,000 within a CD8+ T-cell pool of ~20 × 106 cells, it would require
around 59 × 106 T-DC interactions to achieve 95% recruitment, a number that is largely independent of variations in
precursor frequency within the physiological range. It has been estimated that DCs are able to interact with at least 500
different T cells/hour; thus, a pool of <2000 antigen-presenting DCs could suffice to achieve this near-complete
recruitment.”
Biol 430
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