Self Assessment Answers 11 Asal Biology CB
Self Assessment Answers 11 Asal Biology CB
Self Assessment Answers 11 Asal Biology CB
Coursebook answers
Chapter 11
Self-assessment questions
1 a Antibodies are produced in the body by b 8.5 − 10.0 μm
cells of the immune system.
working
Antibiotics are medicinal drugs that are
produced outside the body and are given width of neutrophil in Figure 11.3
by mouth or by injection. = 50 mm = 50 000 μm
3 a The width of the largest bacterium is 0.8 μm 6 The activation of the specific clones of
lymphocytes only happens when antigens on
working the surface of the pathogen make contact
with the receptors on the surface of B cells.
length of largest bacterium in Figure 11.3 In that sense the pathogen does ‘choose’ the
= 5 mm = 5000 μm lymphocytes that can destroy it. ‘Choose’
suggests that the pathogen actively searches
actual width = 5000 ÷ 6000
out the appropriate lymphocytes, which it
= 0.8 / 1.0 μm does not. The interaction between pathogen
and lymphocytes occurs at random as the
pathogen passes through places where there
are large numbers of lymphocytes, such as in 12 The cytoplasm of plasma cells is full of
the spleen and in the lymph nodes. rough endoplasmic reticulum where protein is
made. There are Golgi bodies for modifying
7 The B cell receptors give each B cell its proteins to become antibody molecules and
specificity. The receptors are proteins with a packaging them into vesicles for exocytosis.
specific shape that is complementary to only The mitochondria provide energy for protein
one antigen. This means that all the B cells with synthesis and for moving vesicles to the
the same specificity (B cell clone) will become cell surface membrane for secretion by
active only when that antigen is detected. In exocytosis.
turn this means that only the B cells with the
greatest chance of producing antibodies that 13 The secondary immune response is faster and
will attach to the pathogen with that antigen produces a higher concentration of antibody
will be produced. This saves resources (amino molecules.
acids needed to make antibodies) and the energy
needed to make them. The discussion should 14 The primary response to an antigen is slow.
build on knowledge of protein structure from It can take several weeks to produce enough
Chapter 2, enzyme–substrate specificity from antibody molecules to fight the infection
Chapter 3 and cell signalling from Chapter 4. effectively. During this time, we usually show
the symptoms of the disease concerned.
8 The analogy must convey the idea that among
a very large group there is a small number of 15 All antibodies have the same constant region
items that are complementary to a specific so they will all be recognised by the same
antigen. receptor on the surface of phagocytes. This
makes it much easier for phagocytes to
An example: anti-virus software looks for a recognise pathogens coated in antibodies all
specific electronic virus that is only found in with different specificities, which means, all
the devices that have been ‘infected’. with different variable regions.
9 Only cells in clone Y have B cell receptors of 16 a Each of the four polypeptides has
the correct specificity. a primary, secondary and tertiary
structure.The secondary and tertiary
10 12.3 μm structures are visible in Figure 11.9. Each
working antibody molecule is composed of four
polypeptides (two heavy and two light);
width of plasma cell in Figure 11.7 as each molecule is composed of more
= 74 mm = 74 000 μm than one polypeptide it shows quaternary
structure. Note that quaternary structure
accept 74 ± 1 mm does not mean that there must be four
polypeptides. Some enzyme molecules have
e.g. actual width = 74 000 ÷ 6000
two polypeptides and they show quaternary
= 12.3 μm structure as well.
T-killer cells and macrophages. The diagram are removed from the circulation. This is
can include cell surface receptors on these cells natural passive immunity.
that are complementary in shape to the shapes
drawn for the cytokines. The fetus does not produce its own
antibodies, because it does not have any
19 a B cells with receptors complementary mature B cells or T cells and develops in a
to the toxin are activated and divide by sterile environment in the uterus. The infant
mitosis to form plasma cells and memory produces its own antibodies shortly after
cells. The plasma cells secrete antitoxins birth as it is infected by microorganisms.
that combine with molecules of the This is natural active immunity.
diphtheria toxin and make it harmless. If
there is another infection, then the memory b The infant is protected against diseases
cells will be activated and there will be a which are endemic and which the mother
much faster secondary immune response. has caught or been vaccinated against. For
example, measles is a serious childhood
b T-killer cells with receptors infection; the infant is protected for
complementary to antigens on the surface several months by its mother’s antibodies.
of the measles virus are activated and (Note that the infant will not gain passive
divide to form a larger clone of cells that immunity to any diseases that the mother
recognise the measles antigens. These has not encountered.)
T-killer cells search for any cells that are
infected with the measles virus and kill 24 People may be immune to a disease because
them so preventing the reproduction of they have many memory cells which can mount
the virus within infected cells in the gas a fast immune response when the pathogen
exchange system. enters their bodies. They can make the specific
antibodies and T cells required to defend
20 Immunity to one strain does not provide themselves immediately the pathogen enters.
immunity to all strains, as they do not all
share the same antigens. A bacterium may be resistant to an antibiotic.
This means that it is able to survive even in the
21 Natural immunity is immunity gained presence of the antibiotic. For example, it may
by being infected (active) or by receiving produce enzymes, such as penicillinases, that
antibodies from the mother across the break down the antibiotic penicillin.
placenta or in breast milk (passive).
25 The primary immune response cannot take
Artificial immunity is immunity gained place as soon as the antigen enters the body.
either by vaccination (active) or by injecting This is because there are very few cells in
antibodies (passive). the B cell and T cell clones that recognise
this specific antigen. First the antigen has
22 Artificial active: antigens are introduced into the to come into contact with the lymphocytes
body by injection or by mouth, and stimulate with cell surface receptors complementary
an immune response by specific B cells and T to the antigen. This takes time as the B and
cells. This provides long-term immunity but is T cells are scattered throughout the body in
not immediate, as the immune response takes the blood and in lymphoid tissue. Once the
several weeks to become effective. specific cells are activated (clonal selection),
it takes time for them to divide by mitosis
Artificial passive: antibodies are injected into
(clonal expansion). Further time is required
the body to give immediate protection against
for B cells to differentiate into plasma cells
a pathogen or toxin. Antibodies are soon
and T-helper cells to secrete cytokines to
removed from circulation and no immune
activate the immune response. Even more
response has occurred, so this is a temporary
time is needed for the plasma cells to carry
form of immunity.
out transcription and translation and secrete
23 a The concentration of maternal antibodies antibody molecules into the blood.
increases during pregnancy as they cross
The secondary immune response can occur
the placenta. The concentration of these
almost immediately as there are many
antibodies decreases after birth as they
memory B cells and memory T cells which
have receptors specific for the antigen. There they will not catch these diseases and will
is a much higher chance that these cells will not require medical treatment. This reduces
recognise the antigen as there are more of the burden on health services.
these cells scattered throughout the body than
was the case before clonal expansion occurred 28 The discussion will probably centre round the
in the primary response. roles of B-lymphocytes and T-lymphocytes
and their specificities for different non-self
26 a The WHO routine immunisation schedule antigens. It may also deal with the difference
can be found at: between active and passive immunity and
between natural and artificial immunity.
https://www.who.int/immunization/policy/
immunization_tables/en/ 29 a
Reflection
Some ideas that could be used in a public health
campaign:
• details of the diseases that are prevented by
vaccination
• severity of these diseases
• deaths caused in recent epidemics linked to
low vaccination rates
• protection of children from diseases that used
to be common in childhood and lead to ill
health and loss of schooling
• protection of whole communities as a result of
herd / mass immunity
• evidence from statistics for immunisation rates
and decrease in incidence / number of cases of
vaccine preventable diseases.