Chapter 11
Immunology
By the end o this chapter you should be able to:
a describe the mode o action o phagocytes;
b describe the roles o mast cells and histamine
production, complement, and phagocytes as
antigen-presenting cells;
c dene the term ‘immune response’;
d compare the origin and maturation o B- and
T-lymphocytes,
T-lymphocytes, including the types o T-cells
and their unctions, and B-cells and their
unctions;
e distinguish between the humoral and the cell-
mediated immune responses;
  explain the role o T- and B-memory cells in
long-term immunity;
Parasites and pathogens
Inectious diseases are ones that we can catch
rom someone else, such as a cold, TB, malaria
and HIV/AIDS. These diseases are caused by
pathogens. A pathogen can be dened as a
microorganism
microor ganism that causes disease.
Pathogens
Patho gens are a kind o parasite
parasite.. A parasite is
an organism that lives in a very close relationship
with another organism, called its host, and does it
harm. The parasite gains rom the relationship
relationship.. So
all pathogens are parasites, but not all parasites
p arasites are
pathogens. For example, you might have lice living
in your hair,
hair, but they are not causing a disease so
they are not pathogens.
A well-adapted parasite or pathogen does not
kill its host. The parasite or pathogen is most likely
to survive, and produce ospring that can move
to a new host, i its host survives long enough or
this to happen. Most o the inectious diseases that
have been around or a long time, such as colds,
measles and TB, either do not kill us – or do not
kill us quickly.
g relate the molecular structure o a typical
antibody molecule to its unction, including
specicity;
h distinguish between active and passive
immunity, natural and articial immunity;
i explain the role o vaccination in providing
providing
immunity;
 j state what is meant by a monoclonal antibody;
k describe the use o monoclonal antibodies in
diagnosis and treatment, including pregnancy
testing, and the anticancer drug MabTher
MabTheraa®.
Pathogens belong to one o our dierent groups
Pathogens
o microorga
microorganisms
nisms – viruses, bacteria, ungi and
protozoa. (Some may argue that viruses are not
organisms at all.) Table 11.1 lists some examples o 
diseases caused by each o these groups.
The immune response
We have numerous deences against invasion o 
our bodies by pathogens. The rst line o deence
is to stop them getting in at all. I they do gain
access, then the immune system comes into action.
The way in which white blood cells respond when
pathogens enter the body is called the immune
response.
Several types o white blood cells (leucocytes)
are able to recognise ‘oreign’ cells or molecules
that enter the body. In other words, they can
distinguish sel rom non-sel.
non-sel. The immune
response is the way in which the immune system
responds to the presence o non-sel cells or
molecules in the body.
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 Chapter 11: Immunology
Pathogen Type o microorganism
human immunodeciency virus virus
(HIV)
adenovirus virus
Mycobacterium bacterium
Tinea pedis ungus
Plasmodium protozoan
Table 11.1 Causes o some inectious diseases.
Primary lines o deence
The best line o deence against pathogens is to
prevent them rom getting established in
the body.
Skin is impermeable
imper meable to most pathogens,
although there are a ew viruses, such as the ones
that cause warts, that can penetrate unbroken
skin. We
We have our own ‘ora’ o harmless
bacteria that live on health
h ealthy
y skin, but most
pathogenic bacteria cannot survive there, partly
because lactic acid and atty acids secreted rom
sweatt glands and sebaceous glands provide a pH
swea
that is too low or them. However, the common
bacterium Staphylococcus aureus can thrive even
on undamaged skin, and it oten inects hair
ollicles and sebaceous glands
glands..
The normal bacterial ora living on our body
suraces can help to prevent inection by other
microorganisms. For example, the bacteria that
normally live in the vagina keep the pH low by
secreting lactic acid. I a person takes antibiotics,
these bacteria may be killed. Then the pH
o the vagina rises, and this may allow other
microorganisms,
microorgani sms, such as the ungus that causes
thrush, Candida
Candida,, to multiply to a much greater
population density than usual.
I skin is damaged – or example, by cuts
or extensive burns – then the way is open or
bacteria to get into the underlying tissues. Blood
clotting helps to seal wounds rapidly,
rapidly, until a
more permanent repair is produced by mitosis
o the cells surrounding the wound. A blood
clot orms when soluble, globular brinogen is
222
Disease caused
acquired immune deciency
syndrome (AIDS)
colds
tuberculosis (TB)
athlete’s oot
malaria
converted to the insoluble, brous protein brin.
This orms a mesh o strands across the wound
in which platelets stick and red blood cells get
trapped, thus preventing urther loss o blood or
entry o pathogens
pathogens..
Moist body suraces, such as the surace o 
the eyes and mouth, are bathed in uids which
have
ha ve some bactericidal action. An enzyme called
lysozyme is present in saliva and tears, and this
enzyme can damage and destro destroy
y many bacteria.
Semen contains a bactericide called spermine;
milk contains a bactericidal enzyme called
lactoperoxidase. The hydrochloric acid secreted
into the stomach is very eective in destroying
destroying
bacteria and other pathogens ingested in ood.
Mucus helps to protect the digestive and
respiratory tracts rom
rom inection. It acts as a
barrier so that bacteria cannot make contact with
the epithelial cells lining the walls o the tubes.
Mucus is produced by goblet cells, which are part
o the epithelium. A layer o cells containing
goblet cells is sometimes known as a mucous
membrane (but don’t conuse this ‘membrane’
with a plasma membrane o a cell). In the trachea
and bronchi, the mucus is swept upwards to the
back o the throat by cilia and then swallowed.
swallowed.
Coughing and sneezing help to expel mucus
containing microorganisms rom the trachea and
bronchi. I the mucus is swallowed,
swallowed, the acid and
enzymes in the stomach destro
destroy
y any bacteria
trapped in it.
 Chapter 11: Immunology

Phagocytes in especially large numbers in the liver, where they

I pathogens do get through the body’s
body’s outer are known as Kuper cells. They also line the
deences, they may be destroyed by patrolling passages through which lymph ows inside lymph
phagocytic white blood cells.
cells. The types o white nodes and are ound on the inside o the alveolar
blood cells known as neutrophils and macrophages walls. Unlike neutrophils, they are quite long-lived,
are phagocytes.
phagocytes. They engul and digest oreign tending to survive ater taking in oreign particles.
particles o almost any type or size (Figure 11.1). They break the particles up into their component
They crawl around
around within almost every part o the molecules and place some o these molecules in
body – or example,
example, over the suraces o the alveoli their plasma membranes. Cells that do this are
in the lungs. called antigen-presenting cells. By doing this, they
Neutrophils are ound in the blood, where display the molecules to other cells o the immune
they make up about 60% o the white blood cells. system, helping these cells to identiy the invaders
They do not live very long, oten dying ater they and be able to destroy them. This role is described
have
ha ve taken in and destro
destroyed
yed bacteria, and so new more ully on pages 226–228.
neutrophils are constantly being made in the For phagocytosis to take place, the
bone marrow. They move around actively, and microorganisms
microorg anisms must rst adhere to the plasma
requently leave
leave the blood and patr
p atrol
ol parts o the membrane o the phagocyte. This process is helped
body where ‘invaders’ may be ound. by a group o proteins called complement (page
Macrophages also leave
leave the blood. (Indeed, 228) which are always present in the blood plasma,
when they are actually in the blood they are given and also by chemicals called cytokines, which are
a dierent name – monocytes.) They are present produced by other white blood cells in response

1 Phagocytic white blood cell

moves towards a pathogen.
2 Phagocytosis takes
place. 3 Lysosomes join with the
vacuole (phagosome) and
the pathogen is killed and
digested.
lysosome phagosome

4  Any chemicals that are

not absorbed into the
cell are egested.

Figure 11.1 Phagocytosis.

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 Chapter 11: Immunology
to the presence o particular antigens. Cytokines
make phagocytes more efcient at killing any
microorganisms that they have enguled.
The way in which phagocytes deal with invading
cells or other oreign material is a non-specic
response. Each phagocyte can attack and destroy
destroy
any type o non-sel material.
Lymphocytes
Lymphocytes are relatively
relatively small white blood
cells.. They are o two types,
cells types, B-lymphocytes and
T-lymphocytes. These two types look identical,
and dier only in their unctions. B-lymphocytes
are so-called because they develop in the bone
marrow, while T-lymphocytes need to spend time
in the thymus gland during a person’s
person’s childhood
to become properly developed. This gland is ound
in the neck. It disappears by the time a person
becomes a teenager
teenager..
Lymphocytes are stimulated into action
when they come into contact with molecules
called antigens. Invading bacteria and viruses
are recognised as oreign because they carry or
produce antigens that are dierent rom any o our
own molecules. Antigens may be ‘ree’ or they may
be part o a bigger structure, such as the cell wall
o a bacterium.
bacterium.
We have a huge number o dierent kinds o  the lymph channels inside a lymph node, holding
lymphocytes in our blood. Each one is capable
o recognising and responding to one particular
antigen. The response o lymphocytes to non-sel  The B-lymphocyte responds by dividing
molecules is thereore known as a specic response.
As they mature, lymphocytes produce small
quantities o particular glycoproteins called
antibodies (page 233). We have perhaps a million
dierent kinds o lymphocytes, each kind
producing an antibody which is slightly dierent
rom other antibodies. At this stage, the antibodies
are placed into the plasma membranes o the
lymphocytes (Figure 11.2). Here, the antibodies act
as receptors, able
able to bind with a particular antigen
i this should appear in the body
body..
I bacteria enter the body,
body, there is a good chance
that some o the lymphocytes will have receptors that
bind with antigens on the surace o the bacteria. I  their particular antibody and release them by
so, then a response is triggered. B-lymphocytes and
T-lymphocytes respond dierently.
224
One type o antibody is held in the
plasma membrane – acting as a
receptor or a specic antigen.
The same antibody
can be secreted rom
the cell in quantity.
Figure 11.2 A lymphocyte can produce one
specic type o antibody
antibody..
How B-lymphocytes respond to antigens
Most B-lymphocytes will spend all their lives
without anything happening to them at all, because
they never meet their particular antigen. But i a
B-lymphocyte does encounter an antigen which
binds to the receptors in its plasma membrane,
it is triggered into action. It could simply meet
this antigen in the blood, or it could meet it as
it is being displayed in the plasma membrane
o an antigen-presenting cell (APC) such as a
macrophage (Figure 11.3).
You can imagine the macrophages sitting in
out the antigens they have discovered so that the
lymphocytes will ‘see’ them as they pass by.
repeatedly by mitosis. A large number o 
genetically identical cells is ormed – a clone o the
stimulated lymphocyte.
The process o the B-lymphocyte binding
with its specic antigen is sometimes called
clonal selection, and its division to orm a clone
o genetically identical cells is called clonal
prolieration or clonal expansion.
Some o these cells dierentiate into plasma
cells. These cells develop extra protein-making
machinery – more endoplasmic reticulum, more
ribosomes and more Golgi apparatus.
apparatus. They
rapidly synthesise more and more molecules o 
exocytosis.. It has been estimated that a plasma cell
exocytosis
can produce and release more than 2000 antibody
 Chapter 11: Immunology

bacterium
phagocytosis by an antigen-presenting
cell (APC), e.g. macrophage

antigen processed
and displayed

The B-lymphocyte The B-lymphocyte meets The B-lymphocyte

displays an antibody its specic antigen either  divides to produce
specic to the antigen on a macrophage or on many plasma cells,
on the bacterium. the bacterium. which all secrete
antibodies.

Figure 11.3 B-lymphocyte response to antigen.

molecules per second. Perhaps as a direct result o  be a macrophage that is displaying some o the
this tremendous rate o activity
activity,, plasma cells do
not live long, mostly disappearing ater only a ew
weeks.
The antibodies are secreted into the blood and
so are carried to all parts o the body. They bind
with the antigens on the invading bacteria, which
results in the destruction o the bacteria – as we
shall see on pages 232 – 233.
Other cells in the clone produced by the original
B-lymphocyte’ss division do not secrete antibodies
B-lymphocyte’ antibodies..
Instead, they remain as memory cells. These cells
live or a long time, and remain circulating in the
blood long ater the invading bacteria have all been
destroyed.
destro yed. They are capable o responding very
quickly i the same type o bacterium enters the
body again.
How T-lymphocytes
T-lymphocytes respond to antigens
T-lymphocytes, like B-lymphocytes, are activated
i and when their particular antigen binds with the
specic glycoproteins that
that are held in their plasma
membranes. T-lymphocytes, however, normally
only respond to their antigen i they nd it in the
plasma membrane o another cell. This could
molecules rom a pathogen that it has taken up.
Or it could be molecules on a body cell that has
been invaded by a virus, and has placed virus
particles in its plasma membrane as a ‘help’ signal
(Figure 11.4).
There are several types o T-l
T-lymphocytes,
ymphocytes,
including T-helper cells and T-killer cells. A
particular T-helper cell with the complementary
receptor binds to the antigen that it has ound. It
then divides to orm a clone o itsel. The cloned
T-helper cells then begin to secrete chemicals called
cytokines. These chemicals stimulate other cells to
ght against the invaders. For example, they may
stimulatee macrophages to carry out phagocytosis
stimulat phagocytosis,,
or they may stimulate
stimulate B-lymphocytes specic to
this antigen to divide rapidly and become plasma
cells. They also help to stimulate appropriate
T-killer cells.
T-killer
T-killer cells actually destro
destroy
y the cell to which
they have become bound. A body cell displaying
virus particles will be destroyed by T-killer cells.
This is the only way o destroying the viruses – it
can’tt be done
can’ d one without destroying the cell in which
they are multiplyi
multiplying.
ng. The T-killer cells destroy
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 Chapter 11: Immunology

 A macrophage The T-lymphocyte

(APC) ingests, meets the specic
processes and antibody on a
displays an antigen. macrophage or 
another APC.

T-helper cells
The T-helper or T-kill
T-killer 
er 
lymphocyte displays on The T-lymphocyte
its plasma membrane divides.
an antibody specic to
the antigen. T-killer cells

T-helper cells secrete

cytokines to stimulate
phagocytic cells and
B-lymphocytes.
 A cell inected by
virus displays the
antigen on its surace.

T-killer cells kill the

cells they attach to.

Figure 11.4 T-lymphocyte

T-lymphocyte response to antigen.

the inected cell by secreting chemicals such as SAQ 

hydrogen peroxide. The T-killer cells are our main
2 Match each o these words with its denition
deence against viral diseases
diseases..
We have seen that T-lymphocytes, like
B-lymphocytes,, divide to orm clones when they
B-lymphocytes
meet their own particular antigen (Figure 11.5).
While most o these cells act as helper cells or
killer cells, some o them remain in the blood as
memory cells. These,
These, like the memory cells ormed
rom B-lymphocytes,
B-lymphocytes, help the body to respond
more quickly and eectively i this same antigen
ever invades again.
SAQ  d an organism that lives in close association
1 With reerence to the way in which they respond
to antigens, suggest why T-lymphocytes are
more eective than B-lymphocytes in dealing
with inection by a virus.
below.
antibody, antigen, pathogen, parasite,
B-lymphocyte, neutrophil, macrophage
a a type o white blood cell that divides
to produce plasma cells, which secrete
antibodies
b a phagocytic white blood cell with a
multilobed nucleus and granular cytoplasm
c a molecule that is recognised by lymphocytes
as being oreign to the body
with a host, and does it harm.
e a microorganism that causes disease
  a glycoprotein secreted by some white blood
cells, which binds to specic antigens
g a phagocytic white blood cell that is
relatively large, and which tends to be ound
in tissues such as the lungs, rather than in
the blood

226
 Chapter 11: Immunology

B-cells T-cells

Specic binding antigen

B-lymphocyte with antibody Antigen presentation
in its plasma membrane  An APC (macrophage)
binds to complementary ingests, processes and
antigen. presents antigen.

Clonal selection and prolieration

Stimulated B-lymphocyte divides
many times.
Specic binding
T-helper lymphocyte or 
T-killer lymphocyte binds to
complementary antigen on
an APC.

Clonal selection and

prolieration
One clone is stimulated
and this T-lymphocyte
divides many times.
Memory cells Plasma cells either 
These survive or  These secrete large
a long time. amounts o antibody.

T-killer lymphocytes T-helper lymphocytes

These bind to cells These secrete cytokines
presenting the which stimulate
I antigen appears later,
complementary antigen. phagocytic cells and
the memory cells are
other lymphocytes.
stimulated, divide and
produce many plasma
cells very quickly
quickly.. memory memory
cells cells
T-killer cells bind
to cells presenting
the complementary
antigen and kill them.

cell killed

Figure 11.5 Summary o B-lymphocyte and T-lymphocyte

T-lymphocyte actions.
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 Chapter 11: Immunology

SAQ  or complements, the activity o antibodies and

3 To answer this question, you will need to think phagocytes.. Complement is very important in
phagocytes
back to your work on cells. ghting bacterial inections
inections..
An experiment was carried out to ollow what
what Many o the proteins that make up complement
happens inside plasma cells as they make and are precursors o enzymes. When a piece o their
secrete antibodies. Some cells were cultured in molecule is removed, they become active active.. Once one
a solution containing amino acids which had o them has been activa
activated
ted in this way,
way, it acts as a
been ‘labelled’ with a radioactive marker. The catalyst or
or the activation o another complement
radioactivity in the Golgi body
body,, endoplasmic protein. This becomes a cascade process, in which
reticulum and ribosomes was then measured one small action (what
(whatever
ever activates the rst
over the next 40 minutes. The results are shown protein) ends up having a very large eect on a
in the graph. large number o protein molecules (Figure 11.6).
There is more than one wa way y in which the cascade
ribosomes cisternae o  can be initiated. Firstly,
Firstly, when an antibody binds
40 endoplasmic
reticulum to an antigen, one o the complement proteins can
  s
   t
   i bind to the antibody. This changes the shape o the
  n Golgi body
  u 30
  y
  r complement protein, activating it and setting o 
  a
  r
   t
   i the cascade. Alternatively, a dierent complement
   b
  r
  a
20 protein can bind directly with a pathogen (or any
   /
  y
   t other ‘non-sel’ surace). Once again, this changes
   i
  v
   i
   t
  c 10 its shape and starts o the cascade. The result
  a
  o
   i
   d
o either o these events is the production o 
  a
   R 0 various proteins that can help to destroy invading
invading
0 10 20 30 40 microorganisms. There are three ways in which
Time / minutes
they do this.
Opsonisation – Some o the proteins produced
produced
a In which order did the amino acids move •
when the complement cascade is activa activated
ted bind
through the three organelles? Use the results
to the surace o bacteria, coating them with
shown in the graph to justiy your answer.
a layer o protein called opsonin. Phagocytic
b Using your own knowledge, describe what
cells have
have receptors which bind to opsonin, and
happened to the amino acids in each organelle.
this stimulates them to engul and destroy the
c Suggest why the peak values or the
coated bacterium.
radioactivity in the ribosomes and the
Attracting macrophages and other cells to
endoplasmic reticulum are the same, whereas •
the site o inection – Some o the newly
the peak value or the Golgi body is lower.
produced complement proteins drit away rom
(There may be more than one possibility.)
the place where they were ormed, into the
d Suggest how the amino acids would have been
tissue uid and blood. Their presence attracts
taken up into the cell at the beginning o the
phagocytes and other white blood cells, which
experiment.
move towards the site. (Cell movement in the
e Describe how the antibody molecules would
direction o a chemical stimulus is is an example
be secreted rom the cell.
o chemotaxis.) This is important in the
inammatory response.
Complement Destroying oreign cells – A third kind o 
•
Complement is a collection o small proteins (more complement protein directly destroys the cells
than 25 dierent ones) that are always present that stimulated
stimulated its production, by making holes
in the blood plasma. It was rst discovered in in their plasma membranes
membranes..
1895, and was given this name because it helps,
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 Chapter 11: Immunology

Complement is a group o short-lived soluble proteins

The active proteins help destroy oreign cells.
always present in blood plasma. Complement is activated
by contact with antibody bound to antigen, or with a
oreign surace. Activation o complement triggers a
cascade which results in the production o active proteins. Opsonins coat a oreign
cell which encourages
activation phagocytosis.

inactive enzyme active enzyme

Phagocytes are
inactive enzyme active enzyme attracted to the
a complement area by active
protein complement protein.
inactive active
complement complement
protein protein

Foreign cells are

destroyed by active
complement protein.

Figure 11.6 Complement.

The infammatory response Mast cells

I a pathogen gets into a particular area o your
body and begins to multiply, it is no use having
your phagocytes and lymphocytes spread all over
the body – you need them to be concentrated in the
danger area. The process that brings this about is
called the infammatory response, and it results in
inammation (Figure 11.7).
Imagine, or example, that a thorn has
penetrated deep under your skin. Bacteria on the
thorn begin to multiply.
multiply. The presence o antigens
on the bacteria, and your own damaged tissues,
tissues,
activate
activa te the complement system. Chemicals are
released that increase the blood supply to the area
and make the capillaries more permeable.
permeable. This
brings more phagocytes and lymphocytes to the
inected tissues. Phagocytes are attracted to the
area by the chemicals, and they crawl out o the
blood into the inected tissues.
The extra blood supply makes the area look red,
and the leakage o uid rom the blood makes it
swollen.
sw ollen. I all goes well, your body will win the
battle against the pathogens,
pathogens, and the swelling and
redness will subside as the inection is brought
under control. Sometimes, a thick white mixture o  into the IgE molecule binds with them, the
dead bacteria, lymphocytes and phagocytes builds
up, known as pus.
Mast cells are cells that are ound in all tissues,
generally lying close to the walls o blood vessels
and nerves. Their cytoplasm is packed ull o 
granules (Figure 11.8), which contain numerous
chemicals, especially histamine and heparin.
We know a lot about mast cells because they are
very much involved in allergies and auto-immune
diseases.. Both o these result rom the immune
diseases
system behaving inappropriately, causing illness.
However, it is also thought that mast cells do
have a useul role to play, probably in helping the
immune system to ght intestinal worms and other
parasites.
Mast cells must be activa
activated
ted beore they begin to
do anything. There are three main ways in which
this happens.
They may respond directly to injury. This could
•
be physical, or it could be caused
cau sed by toxic
chemicals such as alcohol.
The membranes o mast cells have receptors
•
that bind tightly to a type o antibody called
IgE, so each mast cell is completely coated
with IgE molecules. I the protein that ts
IgE molecules become linked together,
together, and
this activates the mast cell. Unortunately, this
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 Chapter 11: Immunology

In an infammation, blood supply to an injured or inected area

is increased. Capillaries in the area become more permeable
allowing more chemicals to leave the blood plasma and enter 
the area. White blood cells crawl out o the capillaries by
chemotaxis.
infammation

tissue damaged by a cut

 Activities taking place at the site o 

injury may include: blood clotting,
Tissue damage and There is greater leakage antibody-antigen interaction,
the presence o  o plasma containing phagocytosis and killing o 
antigens rom bacteria, soluble substances e.g. pathogens.
or example, act as a complement, clotting
stimulus. actors, antibodies. White blood cells are attracted
to the area and leave through
capillary holes in the capillary wall.

 Arterioles supplying capillaries Clotting and immune responses are activated.

dilate, increasing blood fow
into capillaries. This causes the
capillaries to dilate.

Figure 11.7 Inammation.

oten happens not in response to a potentially

dangerous pathogen, but to a harmless antigen
such as a protein in the surace o a pollen
grain, or on a cell in a peanut. These substances
that should be harmless, but that act as antigens
and bring about a strong and inappropriate
immune response, are known as allergens.
Activated
Activa ted complement proteins can also activa
activate
te
•
mast cells.
An activated mast cell releases the contents o 
its granules.
granules. These include histamine and several
cytokines.. These cause an acute inammatory
cytokines
reaction, in which blood vessels dilate,
dilate, smooth
muscle in airways contracts, rashes appear on the
skin and tissues swell as uid accumulates in them.
In a severe allergic reaction, mast cells all over
the body release their contents at the same time,
causing a massive inammatory response that can
nucleus vesicles (granules) mitochondria
that contain histamine be lie-threat
lie-threatening.
ening.
Several diseases are the result o a misdirected
Figure 11.8 A coloured electronmicrograph
electronmicrograph o a attack o the immune system on a person’
person’ss own
mast cell (×12 000). tissues, and these are known as auto-immune
diseases. Mast cells are known to play a major part
230
 Chapter 11: Immunology

in many o these, including rheumatoid arthritis epitope

(in which the joints become inamed) and multiple
sclerosis (in which the myelin sheaths o neurones variable
region
are destroyed). Despite much research, there is
hinge
still no clear picture o what causes these diseases region
to develop.
develop. There does seem to be some genetic
component, because auto-immune diseases may light
have a tendency to run in amilies. However, there chain

is also an environmental component, because the polypeptides

disulphide constant
development o an auto-immune disease oten links region
seems to ollow inection by a virus. polysaccharide
chains

Humoral and cell-mediated responses heavy chain

Early studies o the immune system suggested
that the body had two dierent ways o attacking
pathogens.. One involved cells – the phagocytes and
pathogens
T-lymphocytes
T-lymphocytes – and was called the cell-mediated
response. The other involved chemicals, especially
antibodies produced by B-lymphocytes, and was
called the humoral response. It is now known
that, in reality,
reality, there are constant and complex
interactions between cells and chemicals, as you
will have appreciated rom what you have read
earlier in this chapter.
HIV/AIDS and the immune system
The human immunodeciency virus inects a
particular group o T-helper cells called CD4+
cells, and also some types o macrophages
macrophages.. In the
disease AIDS, the presence o the virus causes
a reduction in the numbers o CD4+ cells. This
can be because the virus itsel destroys the cell as
it reproduces inside it and bursts out rom it; or
because other T-lymphocytes recognise that the
CD4+ cell is inected, and attack and destroy it.
The reduction in numbers o the CD4+ cells
greatly
greatl y weakens the ability o the immune system
to respond to inection, and it is this that causes
the symptoms o AIDS.
Figure 11.9 The structure o an antibody
molecule.
There are several dierent kinds o them, given
names such as IgG and IgA.
Each antibody contains a variable region that
can bind specically with a particular antigen. WeWe
have
ha ve millions o dierent antibodies with dierent
variable
varia ble regions.
regions. The particular part o the antigen
that is recognised by the immune system, and to
which the antibody attaches, is called an epitope.
When an antibody molecule meets its specic
antigen, it binds with it. The eect that this has
depends on what the antigen is, and on what type
o immunoglobulin has bound to it.
Some antibodies directly neutralise the antigen
 – or example,
example, by binding with a toxin
toxin produced
by a bacterium. Others may encourage phagocytes
to destroy the pathogen, sometimes by making the
pathogens clump together. Yet others may stop
pathogens getting a oothold on body suraces, by
preventing them rom attaching to cells or tissues
(Figure 11.10 and Figure 11.11).

Antibodies How immunity develops

Antibodies are glycopr
glycoproteins.
oteins. Their molecules When a pathogen rst enters the body, there will be
contain chains o amino acids, and also sugar only a ew lymphocytes with receptors that t into
units. Figure 11.9 shows the structure o an its antigens. It takes time or these lymphocytes
antibody molecule. to encounter and bind with these pathogens. It
Antibodies are also known as immunoglobulins. takes more time or them to divide to orm clones,
and or the B-lymphocytes to secrete enough
231
 Chapter 11: Immunology

antibody
toxin produced
by bacteria

pathogenic
bacteria
 Antigen binding
stimulates phagocytic
white cells to ingest and
kill the bacterium.
 An antibody can neutralise a
bacterium i the antibody binds
to a chemical necessary or  Toxins released
pathogenicity. by pathogens can
be neutralised by
antibodies.

Figure 11.10 How antibodies neutralise bacteria and bacterial toxins.

I the same pathogen invades again, these memory

cells can mount a much aster and more eective
response.. More antibodies can be produced more
response
antibody with several
sites that can bind to
quickly, usually destroying the pathogen beore it
antigen has caused any illness.
The response to the rst invasion o the
pathogenic
bacterium with pathogen is called the primary response
antigens on its surace (Figure 11.12). Subsequent invasions generate a
secondary response. You can see that the secondary
response happens more quickly
quickly,, and produces
many more antibodies. This is why we usually
The antibody makes the bacteria become immune to a disease i we havehave had it once.
clump together (agglutinate).
 Agglutinated bacteria don't move
around as much and are more Active and passive immunity
readily ingested by phagocytic
white cells.
The kind o immunity described on the previous
pages is a type o  active immunity. The immune
Figure 11.11 How antibodies agglutina
agglutinate
te system has been stimulated to make a particular
bacteria. type o antibody, and can produce this same one
more quickly and in larger quantity i it is exposed
antibodies to destroy the pathogens, or or enough to the same pathogen again. The immunity has
T-lymphocytes
T-lymphocytes to be produced to be able to developed naturally, so it is a type o  natural
destroy
destroy all the cells that are inected by them. immunity.
During this delay, the pathogens have the Another way in which active immunity can
opportunity to divide repeatedly, orming large develop is by vaccination. This invol
involves
ves injecting
populations in the body
b ody tissues.
tissues. The damage that the antigen into the body (page 224). It may, or
they cause, and toxins that they may release, can example, be in the orm o viruses that have
have been
make the person ill. It may be several days, or even made harmless, or as an inactivated toxin rom a
weeks, beore the lymphocytes get on top o the bacterium. The body responds in the same way
pathogen population and destroy it. as it would i inva
invaded
ded by the living pathogen,
However
Howev er,, i the body survives this initial attack producing memory cells which will make the
by the pathogen, memory cells will remain in the person immune to the disease i they should
blood long ater the pathogen
p athogen has been destroyed. ever encounter it. This way o acquiring active
232
 Chapter 11: Immunology

Primary response Secondary response

   d    d
  o   o
  o
   l   o
   l
   b    b
  e   e
   h
   t    h
   t
  n
   i   n
   i
  y   y
   d    d
  o inection   o inection
   b
   i    b
   i
   t    t
  n   n
  a   a
   f    f
  o   o
  n   n
  o
   i   o
   i
   t    t
  a
  r   a
  r
   t    t
  n   n
  e   e
  c   c
  n   n
  o   o
   C    C

weeks or 
years later 
0 1 2 0 1 2 3
Time / weeks Time / weeks

Figure 11.12 Primary and secondary responses to antigen.

immunity is not natural, so it is a orm o  articial
immunity (Figure 11.13).
A young baby’s immune system takes time
to develop. In the uterus, the oetus obtains
antibodies rom the mother’s blood, across the
placenta. Ater birth, the baby will continue to
receive them in the mother’s milk, i she decides
to breasteed. These ready-made antibodies help
the baby to ght o pathogens. The baby has
immunity to the same diseases as the mother.
Because the baby’s body has received ready-made
antibodies, rather
rather than making them itsel, this
is said to be passive immunity. It has happened
naturally, so it is an example o natural immunity
naturally
too.
Passive immunity can also be provi
provided
ded by
injections.. This is not a natural way
injections way o gaining
immunity,, so it is another example o articial
immunity
immunity. For example, i someone goes to the
emergency department o a hospital with a cut that
may have
have dirt in it, they may need to be protected
against the bacterium that causes tetanus
tetanus,,
Clostridium tetani. It is too late or a vaccination,
because by the time the person’s immune system
responds, the bacterium could ha have
ve multiplied
and caused the atal illness tetanus. Instead, the

Active immunity Passive immunity

Immunity developed ater contacting Immunity provided by antibodies or 
pathogens inside the body. antitoxins provided rom outside the body.

Natural Articial Natural Articial

inection injection o live or  antibodies rom a injection o antibodies
attenuated pathogen mother in breast milk or antitoxin
or across the placenta

Figure 11.13 Active and passive immunity.

233
 Chapter 11: Immunology

person will be given an injection o antitoxin. The attenuated (weakened) orm

antitoxin will bind to the toxin produced by the
bacteria, rendering it har mless
mless.. Antitoxins can also
be given in this way to destroy toxins introduced
into the body through bites rom poisonous
animals, such as spiders or snakes
snakes..
Passive immunity
immunity does not last as long as active
immunity. No lymphocytes have been stimulated
to make clones o themselves, so no memory cells
have been ormed. Passive immunity lasts only as
long as the antibodies or antitoxins last. The body
actually ‘sees’ them as being oreign, and they will
be removed and destroyed quite quickly by cells in
the liver and spleen.
Vaccination
Vaccination is an excellent way o preventing a
person rom acquiring an inectious disease. The
larger the proportion o people who are vaccinated
in a population, the lower the chance that anyone
anyone –  wanted to be able to obtain large amounts o one
even those who have
have not been vaccinated – will get
that disease. This is called herd immunity. For most
diseases, at least 80–85% o the population need to
be vaccinated to achieve herd immunity.
Vaccination involves
involves giving a person a dose
do se o  a particular type o B plasma cell, all secreting
a preparation that will cause the immune system
to react as though an antigen rom a pathogenic
organism has entered the body. Most vaccinations
are given by injection, but the polio vaccine
is given by mouth. Many vaccines contain an
attenuated orm o the bacterium or
virus that causes the disease, while others contain a
modied toxin produced by them.
When the vaccine enters the body,
body, lymphocytes
that recognise the antigen respond to it as i 
they had encountered live bacteria or viruses
viruses..
They orm clones o plasma cells, which secrete
antibodies, and also memory cells
cells.. In most cases, a
second ‘booster’ dose o the vaccine is given later
on. This raises the antibody level much higher than
the rst dose, and helps to ensure that protection
against the antigen lasts or some time (Figure
11.14).
Monoclonal antibodies
We have seen that there is a huge number o 
dierent antibodies that can be made by human
B-lymphocytes,, and that each lymphocyte can
B-lymphocytes
make only one kind. In the 1970s, researchers
researchers
particular antibody at a time, so that they could
study it without intererence rom all the other
antibodies that are usually present in a mammal’s
blood. Their aim was to produce a large clone o 
identical antibodies, known as monoclonal
antibodies.
There is one problem in achieving this – 
B-lymphocytes that divide to orm clones o 
plasma cells do not secrete antibodies, and plasma

rst vaccination

booster vaccination booster vaccination at some

a ew weeks later  point in the uture

  y
   d
  o
   b
   i protective level
   t
  n
  a
   f
  o
   l
  e
  v
  e
   L

0 2 4 6 8
Time / months Time

Figure 11.14 Antibody levels ater vaccination.

234
 Chapter 11: Immunology

cells that secrete antibodies do not divide. In 1975, blood clots, in the patient’s body.
a technique was developed to get around this A very dierent diagnostic application is in
problem (Figure 11.15). B-lymphocytes were used testing or pregnancy. Any couple who are trying
with cancer cells, which – unlike other body cells or a baby will want to know as soon as possible
 – go on dividing indenitely.
indenitely. The product o this i the woman has become pregnant. There are
usion is called a hybridoma cell. The hybridoma now many dierent pregnancy testing kits on
divides repeatedly to orm a clone o cells that the market which can be used at home. Most o 
secrete monoclonal antibodies
antibodies.. them use monoclonal antibodies to test or the
When this technique was rst invented, no- presence o a hormone called human chorionic
one really knew what uses might be made o it. gonadotrophin (HCG) in her urine. This hormone
Since then, many applications have been ound is only secreted during pregnancy.
or monoclonal antibodies, both in research and Monoclonal antibodies are made, using mouse
in various areas such as medical diagnosis and lymphocytes, that will bind specically with HCG.
treatment. Their uses derive rom the act that In one type o pregnancy-testing kit, these HCG-
any particular monoclonal antibody binds very specic antibodies are bound to atoms o gold.
specically to a particular molecule. The antibody–gold complexes are then used to
coat the end o a dipstick (Figure 11.16). Another
Using monoclonal antibodies or  type o monoclonal antibody is also made, which
diagnosis
Monoclonal antibodies can be used to help to
antigen injection
diagnose a particular condition, or to nd out
where particular types o cells are present in
the body.
Monoclonal antibodies can be used to locate
places where blood clots hahave
ve ormed in the body
o a person suspected o suering rom deep-vein
thrombosis (a blood clot in a vein, oten in the
leg). First, a mouse is injected with human brin,
a protein ound in blood clots. The brin acts as spleen cells cancer cells
an antigen in the mouse. Mouse B-lymphocytes
B-lymphocytes
mixed and
with the antibody or human brin prolierate,
prolierate, treated to cause
especially in the spleen. Ater a month or so, cell usion

the spleen contains large quantities o these hybridoma cells

lymphocytes.
The mouse spleen cells are then mixed with Tiny samples are taken so that
only one cell is present in a
cancer cells to orm hybridomas,
hybridomas, which are well. The wells are tested to
checked to see which antibody they secrete. nd a hybridoma cell producing
the required antibody.
Hybridomas secreting the anti-brin antibody are
selected and cultured in a ermenter
ermenter,, so that large
amounts o the antibody are made. The antibody
can be ‘labelled’ by
by attaching it to a radioactive
chemical that produces gamma radiation.
The labelled antibodies are then introduced into The hybridoma cell which produces the required
antibody is allowed to divide and produce a clone.
the patient’s
patient’s blood. As they are carried around These cells can be cultured in ermenters, where
the body in the blood stream, they bind to brin they will secrete monoclonal antibody.

molecules.. A gamma camera can be used to detect

molecules
the position o the antibodies, an thereore o any Figure 11.15 Monoclonal antibody production.
235
 Chapter 11: Immunology

will specically bind with HCG–antibody–gold brand) builds up.

complexes.. These antibodies are impregnated into
complexes
a region urther up the dipstick, called the Patient
Test Result region.
To use the dipstick, it is dipped into a urine
sample. Any
Any HCG in the urine will bind to the
antibodies at the end o the stick, which will be
carried upwards as the urine seeps up the stick.
As the HCG–antibody–gold complexes reach the
test result region o the stick, they bind with the
antibodies there and are held rmly in position.
As more and more gold atoms arrive there,there, a
pink colour (or another colour
colour,, dependent on the
The stick also contains an area called the
Procedural Control Region, which contains yet
another type o immobilised monoclonal antibody.
antibody.
These are rom goats, and they are anti-mouse
antibodies.. They bind with the antibody–gold
antibodies
complexes even i these have
have not encountered any
HCG in the urine sample. This strip thereore
thereore goes
pink even i the test result is negative.
negative.
Other uses are or producing reagents used
to determine a person’s blood group, the
identication and location o some types o cancer
and ollowing the progression
progression o an HIV inection.

The de
desig
ign
n o
o th
the dipstic
ick
k How th
the pregnancy di
dipstick wo
works

1 The stick is dipped 2 HCG-specic

into urine to the line. antibodies bound to
gold are carried up.
Procedural Control I there is any HCG
Region (antibodies present, it binds to the
specic to the antibodies and is also
antibodies at the carried up.
end o the stick)

Patient Test Region

(immobilised antibody
specic to HCG)

antibodies specic to
HCG bound to gold

3 I the stick is working, a 4 I the urine contains HCG,

pink line always appears
in the Procedural Control
Region – HCG-specic
antibody bound to gold
is carried upwards and
captured by antibody
specic to it, which was
immobilised here.
it binds to the HCG-specic
antibody and gold at the end
o the dipstick and is carried
upwards. When this meets
immobilised HCG-specic
antibody, it is bound and a pink
line appears. This shows the
person is pregnant.

Figure 11.16 How one type o pregnancy-testing kit works.

works.

236
 Chapter 11: Immunology

SAQ Rituximab is used to treat a cancer called

4 Suggest the purpose o the Procedural Control
Region on the pregnancy test dip stick.
Using monoclonal antibodies or  lymph nodes. The drug kills both the abnormal
treatment
The anticancer drug MabThera® is a monoclonal
antibody. MabThera® is a trade name or the drug
rituximab.
Rituximab is a monoclonal antibody that binds
to a protein called CD20. This protein is ound
only on the surace o B-lymphocytes
B-lymphocytes.. When
rituximab binds to these lymphocytes, it destroys
them, although the exact mechanism by which it
does this is not yet understood.
Rituximab
non-Hodgkin lymphoma, in which it is the
B-lymphocytes that are the cancerous cells,
dividing out o control and producing very large
numbers in the body. They orm tumours in the
(cancerous) B-lymphocytes and also any normal
ones, because all o them have CD20 on their
suraces. However, the body continues to produce
new B-lymphocytes which are usually normal,
rather than cancerous, ones.
Rituximab
Rituxima b is also used
u sed to treat some
auto-immune diseases in which overactive
overactive
B-lymphocytes are implicated, such as rheumatoid
arthritis.

Summary
The body’s immune system responds to the presence o non-sel cells or molecules by attacking the
•
oreign material.
material. This is done by various white blood cells (leucocytes), including phagocytes and
lymphocytes.. This response is called the immune response.
lymphocytes response. A molecule that initiates an immune
response is called an antigen.
Phagocytes are mobile cells that are ound in almost all parts o the body. They engul and digest
•
oreign cells or other materials. They include neutrophils and macrophages
macrophages.. Phagocytes oten act as
antigen-presenting cells, placing antigens rom the oreign cells they ha
have
ve enguled in their plasma
membranes,, where other cells o the immune system may come into contact with them.
membranes
Lymphocytes are cells that exist in many dierent varieties.
varieties. Unlike phagocytes, each individual
•
lymphocyte is able to respond only to one particular antigen.
When a B-lymphocyte meets its specic antigen, it responds by dividing to orm a clone o 
•
genetically identical plasma cells. These all secrete antibodies that bind to the antigen.
When a T-lymphocyte meets its specic antigen on the surace o an antigen-presenting cell, it
•
responds by dividing to orm a clone o T-helper cells or T-killer cells.
cells. T-helper cells bind to the
antigen and secrete cytokines, which stimulate
stimulate other cells to attack the antigen. T-killer cells also
bind to the antigen, and then destroy the cell on which the antigen is present.
Both B-lymphocytes and T-lymphocytes also ormorm clones o memory cells, which remain in the body
•
and are able to mount a rapid attack i the same antigen invades the body again.
The blood plasma contains numerous small protein molecules which together orm complement.
•
When antigens are present in the body, the complement system is activated. The shape o one o 
the proteins is altered, causing it to become active as an enzyme and remove part o the molecule o 
another o the complement proteins.
proteins. This activates the second protein, and so on down the chain,
eventually producing large quantities o proteins that help to destroy invading pathogens.
pathogens.

continued ...

237
 Chapter 11: Immunology

Mast cells contain granules o substances such as heparin and histamine. When activated,
activated, they
•
release their granules and this causes inammation to occur. The inammatory response inv involves
olves
the dilation o blood vessels, bringing more lymphocytes and phagocytes to the area. Although mast
cells may have a useul role to play, they are involved in inappropriate immune responses to harmless
substances, called allergens.
allergens. They are also inv
involved
olved in some auto-immune diseases.
HIV invades a particular type o T-lymphocyte called CD4+ cells. This eventually destroys these cells,
T-lymphocyte
•
weakening the immune system and allowing other pathogens to prolierate in the body.
body.
Antibodies are glycoproteins.
glycoproteins. They are also known as immunoglob
immunoglobulins
ulins.. Most o them are Y-shaped
Y-shaped
•
molecules, with binding sites or specic antigens at the tips o the Y.
Y.
Active immunity develops when
when a person’s body
body has responded to the presence o an antigen, and
•
has produced a clone o memory cells that can react promptly i the same antigen invades again.
This can be achieved through natural exposure to the antigen (natural active immunity)
immunity) or through
vaccination (articial active immunity).
Passive immunity develops when antibodies rom elsewhere are introduced into the body. Babies
•
acquire antibodies rom their mother through the placenta and in breast milk (natural passive
immunity). Antibodies may also be injected into the body (articial passive immunity). Passive
immunity does not last as long as active immunity,
immunity, because there are no memory cells involved.
Monoclonal antibodies are identical antibodies produced rom a clone o hybridoma cells.cells. These are
•
produced by using a lymphocyte with a cancer cell. Monoclonal antibodies can be used in diagnosis
(e.g.
(e. MabThera® or the treatment o non-
g. in pregnancy tests) or in the treatment o diseases (e.g. MabThera
Hodgkin lymphoma and rheumatoid arthritis).

Questions
Multiple choice questions
1 The ollowing are the steps involved
involved in the process o phagocytosis o a bacterium by a macrophage.
I recognition and attachment o bacterium to the phagocyte
II attraction o the bacterium and movement o the phagocyte by chemotaxis
III intracellular killing and digestion o bacterium
IV egestion o epitopes and antigen presentation
V usion o lysosome with a vesicle produced by endocytosis (phagosome)
VI engulment o the bacterium by phagocyte
Which o the ollowing shows
shows the correct sequence o the process o phagocytosis?
A I → II → III → IV V
→ →VI
B II → III → I→ IV V
→ →VI
C IV → II → I→ III VI
→ → V
D II → I → VI → V → III →IV

continued ...

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 Chapter 11: Immunology

2 An immune response is best dened as:

A a deensive reaction by the immune system.
B a bodily deence reaction which recognises an invading substance and produces a range o 
cellular and chemical agents directed at the substance.
C a reaction which recognises an invading substance.
substance.
D the body’s reaction to inection.
3 The diagram shows the origin and maturation o B and T-lymphocytes.
T-lymphocytes.

bone marrow
stem cell

lymphoid
precursor cell

matures in thymus matures in bone marrow

II III IV

Which o the ollowing correctly

correctly identies cells I, II, III and IV?

I II III IV
A T-cells B-cells plasma cells memory cells
B plasma cells memory cells B-cells T-cells
C B-cells T-cells plasma cells memory cells
D memory cells plasma cells B-cells T-cells

4 Which o the ollowing parts o statements are correct about cell-mediated

cell-mediated and
humoral immunity?

Cell-mediated Humoral
A involves T-killer cells involves B-cells
B involves B-cells involves T-killer cells
C produces antibodies produces antibodies
D does not involv
involvee cell-to-cell
cell-to-cell interaction
interaction involves
involves cell-to-cell
cell-to-cell interaction
continued ...

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 Chapter 11: Immunology

5 Why is passive immunity eective or only a short time?

A Memory cells are produced.
B Antibodies are broken down rapidly.
C Antigens enter the body.
D Plasma cells are stimula
stimulated.
ted.
6 Students in a class were exposed to the chicken pox virus by an inected student. What type o 
immunity would the students obtain i they also became inected?
A articial active immunity
B articial passive immunity
C natural active immunity
D natural passive immunity
7 Which o the ollowing is not true about antibodies? They:
A neutralise toxins.
B bind to specic antigens
antigens..
C activa
activate
te the complement system.
D are eective only when attached to the T-cells.
8 Immune responses may be specic or non-specic. Which response is a specic immune response?
A capillaries becoming ‘leaky’
B phagocytosis
C release o histamines
D production o memory cells
9 Any o the highly specic antibodies produced in large quantity by the clones o a single hybrid cell
ormed in the laboratory by the usion o a B cell with a tumour cell are known as:
A IgG antibodies.
B monoclonal antibodies
antibodies..
C IgM antibodies.
D IgA antibodies.
10 Monoclonal antibodies are used in all o the ollowing except:
A blood typing or transusions.
transusions.
B the identication o the location o some types o cancer.
C the stimulation o the immune system.
D ollo
ollowing
wing the progression o HIV inection.

continued ...

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 Chapter 11: Immunology

Structured questions
11 a i Wha
Whatt do you understand by the term ‘non-specic immunity’? [1 mark]
ii Give two examples o non-specic immunity
immunity.. [2 marks]
b The diagram below shows the events occurring during a non-specic response
response..

bacteria in cut skin

mast cell

cell 3

produces
substance
cell 1

capillary cell 2

i Name the substance produced by the mast cell. [1 mark]

ii What are the unctions o the substance identied in b i? [2 marks]
iiiIdentiy cells 1, 2 and 3. [2 marks]
iv Explain the role o the complement system in non-specic immunity
immunity.. [3 marks]
v I the inection lasts or a while the specic immune system is stimulated.
Whatt do you understand by the term ‘specic immunity’?
Wha [1 mark]
vi Explain the role o cell 3 in stimulat
stimulating
ing the specic immune system. [3 marks]

continued ...

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 Chapter 11: Immunology

12 The diagram below shows the structure o an antibody.

antibody.

a Name the type o cell that produces antibodies

antibodies.. [1 mark]
b Copy the diagram above
above and label the ollowing parts o an antibody:
binding site, variable
variable region, constant region, disulphide bonds, light chain,
heavy
hea vy chain, hinge region [3 marks]
c State one unction or
or each o the ollowing
ollowing parts:
parts: hinge region and disulphide bonds.
bonds. [2 mar
marks]
ks]
d Explain whwhyy a variab
variable
le region is necessary in the structure o the molecule
molecule.. [1 mark]
e Vaccines contain the antigens o pathogens
pathogens.. There are two types o polio vaccine.
The Salk vaccine contains dead viral particles while the Sabin vaccine is made o a live
attenuated
attenuated polio virus
virus.. The Sabin vaccine replaced the Salk vaccine.
i Wha
Whatt do you understand by the term ‘antigen’? [1 mark]
ii State one advanta
advantage
ge o using living atten
attenuated
uated viruses to make a vaccine
vaccine.. [2 marks]
  The graph below shows the concentration o antibody in the blood o a baby ater the
rst oral vaccine and booster shot or polio.

secondary
   d response
  o
  o
   l
   b
  n
   i
  y
   d
  o
   b
   i
   t
  n
  a
   f
  o
  n primary
  o
   i
   t
  a response
  r
   t
  n
  e
  c
  n
  o
   C

0 10 20 30 40 0 10 20 30 40
delay
rst oral second oral
vaccine vaccine
Time / days

continued ...

242
 Chapter 11: Immunology

i Why is there a delay between the time o the rst oral vaccine and the rst
appearance o antibodies in the blood? [2 marks]
ii State two way
wayss in which the immune system’s primary response diers rom the
secondary response. [2 marks]
iii Explain the dierences shown between the primary and secondary responses
responses.. [2 marks]
13 a Distinguish between:
i natural and articial immunity
ii active and passive immunity. [4 marks]
b Copy and complete the table below to indicate the type o immunity attained in
each case.

Example Type o immunity

baby eeding on breast milk
child exposed to a riend with chicken pox
receiving the MMR vaccine as a child
receiving the H1N1 vaccine as an adult
ad ult
getting an emergency tetanus injection ater
stepping on a rusty nail
[5 marks]
c Describe how an eective vaccine can provide long-term immunity
immunity.. [4 marks]
d Explain how passive immunity provides
provides protection to a person who has been
bitten by a snake. [2 marks]
Essay questions
14 a Describe the mode o action o phagocytes
phagocytes.. [3 marks]
b Dene the term ‘immune response’. [2 marks]
c i Describe the origin and matura
maturation
tion o T-l
T-lymphocytes.
ymphocytes. [2 marks]
ii Describe the changes that occur to T-l
T-lymphocytes
ymphocytes during an immune response
response.. [3 marks]
d i Describe how B-lymphocytes are invol
involved
ved in the immune response. [3 marks]
ii Describe the importance o B memory cells in immunity
immunity.. [2 marks]
15 a i Dene the term ‘antibody’. [1 mark]
ii Make an annotated schematic dra
drawing
wing o an antibody molecule. [4 marks]
iii Describe how an antibody acts on bacteria. [2 marks]
b i Whatt are monoclonal antibodies?
Wha [2 marks]
ii Monoclonal antibodies are used or diagnosis and treatment. Identiy two examples
o each use. [2 marks]
iii Describe the use o monoclonal antibodies in pregnancy kits
kits.. [4 marks]
16 a Distinguish between humoral and cell-mediated immunity
immunity.. [3 marks]
b Dra
Draww a ow diagram to illustrate the stages o the immune response to an
invading
invading pathogen. [7 marks]
c Explain what is meant by clonal selection and clonal expansion. [5 marks]

243