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MOLECULAR BIOLOGY OF THE CELL, SIXTH EDITION CHAPTER 24: THE INNATE AND ADAPTIVE IMMUNE SYSTEMS

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MOLECULAR BIOLOGY OF THE CELL, SIXTH EDITION CHAPTER 24: THE INNATE AND ADAPTIVE IMMUNE SYSTEMS

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MOLECULAR BIOLOGY
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MOLECULAR BIOLOGY










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MOLECULAR BIOLOGY
Grado
MOLECULAR BIOLOGY

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Subido en
6 de diciembre de 2025
Número de páginas
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Escrito en
2025/2026
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MOLECULAR BIOLOGY OF THE CELL, SIXTH EDITION
CHAPTER 24: THE INNATE AND ADAPTIVE IMMUNE
SYSTEMS

1. Indicate whether each of the following descriptions better applies to an adaptive (A) or
innate (I) immune response. Your answer would be a four-letter string composed of letters A and
I only, e.g. AAAA.
( ) It is found in invertebrate and vertebrate animals as well as in plants.
( ) It has a long-lasting memory.
( ) It is highly specific to the particular invading pathogen.
( ) It employs natural killer (NK) cells to induce apoptosis in infected host cells.

2. Which of the following cell types is NOT phagocytic?
A. Macrophage
B. Monocyte
C. Neutrophil
D. Lymphocyte
E. Dendritic cell


3. Blood-group compatibility is an important consideration in red blood cell transfusions
that are administered in millions of liters worldwide every year. In the ABO blood-group system,
individuals with AB blood type are the universal recipient (can accept blood from any donor),
while those with O type are universal donors. If an incompatible transfusion is made between an
A-type (donor) and a B-type (recipient) individual, for example, the anti-A antibodies present in
the recipient’s plasma would rapidly destroy the transfused blood cells with the help of the
complement system, with potentially serious consequences. But why do we produce antibodies
against other blood-group antigens even without having been exposed to those foreign blood
cells before? It has been suggested that these antibodies are generated in response to minor
infections (in early life) with microbes of the normal flora of our bodies, and that, in addition to
binding to the microbial antigens, these antibodies can cross-react with the similar A- and B-type
carbohydrate antigens of the ABO blood-group system. If this is indeed the case, blood plasma
from a “germ-free” individual would react with …
A. blood of any ABO type.
B. blood of no other ABO type.
C. blood from O-type individuals only.

, D. blood from non-O-type individuals only.
E. blood from AB-type individuals only.


4. Which of the following are recognized by pattern recognition receptors as pathogen-
associated molecular patterns?
A. Double-stranded viral RNAs
B. Formylmethionine-containing proteins
C. Unmethylated CpG motifs
D. Bacterial flagella components
E. All of the above


5. Which of the following groups of proteins are pattern recognition receptors?
A. NOD-like receptors
B. Toll-like receptors
C. RIG-like receptors
D. C-type lectin receptors
E. All of the above


6. Gout patients have high uric acid levels in their blood and suffer from arthritis in their
joints as a result of formation of intracellular and extracellular uric acid crystals. Would you
expect treatment with glucocorticoids (G), which inhibit prostaglandin synthesis, or with tumor
necrosis factor (TNF) to be normally used to treat such patients?


7. Indicate whether each of the following descriptions is shared (S) or not shared (N)
between macrophages and neutrophils in destroying invading pathogens in vertebrates. Your
answer would be a four-letter string composed of letters S and N only, e.g. SSSS.
( ) They use a respiratory burst and create toxic reactive oxygen species to kill engulfed
pathogens.
( ) They are normally found in most tissues even before pathogen invasion.
( ) They are long-lived and normally survive long after activation.
( ) They secrete pro-inflammatory cytokines upon encountering invading pathogens.


8. Indicate true (T) and false (F) statements below regarding the complement system. Your
answer would be a four-letter string composed of letters T and F only, e.g. TTFT.
( ) The early complement components form the membrane attack complex, whereas the
late complement components cleave and activate C3.

, ( ) The classical pathway of complement activation is triggered by binding of a secreted
PRR to mannose-containing glycoproteins or glycolipids on the surface of pathogens.
( ) Some pathogens such as Neisseria gonorrhoeae hide from the complement reaction
via sialic acid camouflage.
( ) Once a membrane attack complex is formed, it can attack multiple pathogens before
becoming inactivated.


9. A cell has been infected with an RNA virus. As a consequence, it may …
A. reduce the expression of its surface class I MHC molecules.
B. secrete type I interferons such as interferon-α.
C. shut down most protein translation and destroy most of its RNA.
D. be induced to die by apoptosis.
E. All of the above.


10. Consider two receptors, one inhibitory and one activating, on the surface of natural killer
(NK) cells: KIR receptors that interact with certain class I MHC proteins, and special Fc
receptors that recognize the tail region of IgG antibodies. When NK cells are incubated with an
immortalized B cell line derived by infection of human B cells with Epstein–Barr Virus, the B
cells are killed by NK cells. Normal B cells, in contrast, are not efficiently killed by NK cells. In
each of the following scenarios, indicate whether the described changes are expected to enhance
(E) or suppress (S) the cytotoxicity (killing activity) of the NK cells in this system. Your answer
would be a four-letter string composed of letters E and S only, e.g. SEEE.
( ) The cell line is transformed with human class I MHC genes, and the genes are
expressed.
( ) An anti-CD23 IgG antibody is added to the cells. (CD23 is a known marker on the
surface of the immortalized B cells.)
( ) The cells are treated with stibogluconate, an inhibitor of KIR receptor signaling.
( ) Type I interferons are added to the cells.


11. How are natural killer (NK) cells different from cytotoxic T (TC) cells?
A. NK cells induce apoptosis in their target cells, whereas TC cells are professional
phagocytes.
B. NK cells kill virus-infected cells, whereas TC cells kill cancerous cells.
C. NK cells kill cells with a high level of class I MHC protein expression, whereas
killing by TC cells requires low expression levels.
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