11 Immunity

11.1 The immune system • during an infection (caused by pathogens invading the
body), cells under attack respond by releasing
chemicals called histamines
• these attract neutrophils
• this movement towards chemical stimulus is called
chemotaxis

General steps of phagocytosis

1) attraction (chemotaxis)
2) recognition and attachment
3) endocytosis
4) bacteria trapped within a phagocytotic vacuole
5) fusion of lysosomes and phagocytotic vacuole
6) killing and digestion

Lymphocytes
Phagocytes (neutrophils & macrophages)
• originate in bone marrow
• they’re scavengers – removing any dead cells and
invasive microorganisms

Neutrophils
• have a lobed nucleus and granular cytoplasm
B-cells
• short-lived cells
• made and mature in the bone marrow
Macrophages • travel to the spleen for final stages of maturation
• larger than neutrophils
1) B-plasma cells
• travel in blood as monocytes which develop into
• short-lived
macrophages once they leave blood and settle in
organs, removing foreign matter there • produce antibodies
• long-lived cells
2) B-memory cells
• do not destroy pathogens completely, they’re cut up
and their antigens are displayed, hence it becomes an • form the immunological memory of the body
antigen presenting cell (APC) • responsible for 2° response

Phagocytosis T-cells
Made in the bone marrow but mature in thymus.

Image: Timonina / Shutterstock Image: https://biologydictionary.net/thymus-gland/

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Thelper • they can also increase the effect of phagocytosis
• produce interleukins Þ T-lymphocytes can only recognise antigens on an
• interleukins stimulate: APC surface
1) B-cells to make antibodies
2) other T-cells to divide b) Humoral immunity
3) macrophages to enhance the effect of
phagocytosis

Tkiller (cytotoxic)
• destroys cells by releasing perforin which makes holes
in the cell surface membrane

Tmemory
• leads to immunological memory of antigen
• responsible for 2° response Image: https://www.researchgate.net/

a) Clonal selection
Immunity Process by which an antigen selectively binds to and
activates only those lymphocytes bearing receptors for
the antigen. In short, this is basically recognising and
choosing which B-cells to use.
• Thelper cell recognises B-APC and becomes activated,
releasing interleukins to signal further actions

b) Clonal expansion (proliferation)

a) Cell-mediated immunity
The rapid multiplication of B (or T) cell clones after
This is where T-lymphocytes respond to altered cells activation by an antigen.
(APC, cancer cells, cells that’ve been infected by viruses)
• B-APC divides and differentiates into –
1) plasma cells to make specific antibodies
2) memory cells to prepare for 2° response

Þ B-cells can respond to APC as well as pathogens

directly

Numbers of white blood cells

• Neutrophils in the blood increases during bacterial
infections and whenever tissues become inflamed and
die
• Lymphocyte numbers increase during viral infections
and TB

Image: www.macmillanhighered.com

1) macrophage engulfs pathogen and becomes an APC

2) Thelper’s cell receptor, which is complementary to the
antigen, binds to antigen on APC • leukaemias are cancers of these stem cells
3) Thelper then releases interleukins • cells divide uncontrollably to produce many cells that
• interleukins stimulate B-cells to divide into plasma don’t differentiate properly and disrupt production of
cells and produce antibodies in the humoral normal blood cells
response

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 Autoimmune diseases
Occurs when the immune system mistakenly identifies
self-antigens as foreign (non-self) and mounts an
immune response against them.
• during the maturation of T-cells in the thymus, millions
of cells are destroyed as they have T-cell receptors
complementary to self-antigens
• some of these cells evade destruction and are
activated to stimulate an immune response against
the body’s own proteins
• starts as an attack involving antibodies and killer T-
cells against certain parts of the body
• attack can be localised in one organ or directed
Image: https://orthoinfo.aaos.org/en/diseases--conditions/leukemia/ against the whole body
• immature white blood cells are produced quickly, • e.g., Myasthenia gravis, rheumatoid arthritis, type 1
disrupting balance of components in blood diabetes, lupus, psoriasis, etc.
• as a result, the body does not have enough red blood
cells or platelets Myasthenia gravis (MG)
• this causes anaemia and increases the risk of
excessive bleeding
• the number of mature lymphocytes and neutrophils
decrease, so susceptibility to infections increase
• the person is now said to be immunosuppressed

Immune response
> immune response – the complex series of responses
of the body to the entry of a foreign antigen
- involves the activity of lymphocytes and
phagocytes
Image: https://healthjade.com/acetylcholine/

• antigen – substance that is foreign to the body and • antibodies are produced against receptors on muscle
stimulates an immune response fibres for acetylcholine which is released by ends of
• self – substance produced by the body that the motor neurones to stimulate muscle contraction
immune system does not recognise as foreign and • people with MG have Thelper cells that are specific for
therefore does not stimulate an immune response cell surface receptors for acetylcholine
• non-self – any substance or cell recognised by the • Thelper cells stimulate a clone of B-cells to differentiate
immune system as foreign and stimulates an immune into plasma cells and secrete antibodies that bind to
response receptor blocking transmission from motor neurones
• muscle cells are not stimulated so muscle tissue
Role of memory cells in long-term immunity starts to break down

Remain in the blood for years and cause long-term • symptoms – muscle weakness
protection. • treatment – drug that inhibits enzyme in synapses
that breaks down acetylcholine increases its
concentration so its action in stimulating muscle
contraction lasts longer or surgical removal of the
thymus gland

11.2 Antibodies and vaccination

Antibodies
• globular glycoproteins
• have quaternary structure
• form group of plasma proteins called
immunoglobulins
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 Using monoclonal antibodies in diagnosis and
treatment of disease
In diagnosis
• used to locate position of blood clots
• used to locate cancer cells which have different cell
surface proteins and therefore can be detected by
antibodies
• used to identify exact strain of virus or bacterium
causing an infection, which speeds up treatment

In treatment
• treatment of breast cancer – antibody binds to
cancerous cells and marks them for destruction by
• Hinge region – gives flexibility to bind around antigen immune system
• treatment of rheumatoid arthritis (autoimmune) –
• Antigen binding sites – sequence of amino acids in
antibody binds to proteins secreted by T-cells that
these regions make a specific 3D shape which binds
causes damage to cartilage in joints and blocks its
to one type of antigen
action

Functions of antibodies Types of immunity

• attach to flagella of bacteria making them less active

and easier for phagocytes to engulf
• cause agglutination (clumping together) of bacteria,
reducing chances of spread
• punch holes in bacteria cell walls, causing them to
burst when they absorb water by osmosis
• antibodies coat bacteria, making phagocytosis easier
as phagocytes have receptor proteins
• combine with toxins, neutralising them (antitoxins)
• combine with viruses and bacterial toxins, preventing
them from entering or damaging cells
Vaccination
Vaccines
Hybridoma method for the production of • preparation containing antigens which is used to
monoclonal antibodies stimulate an immune response artificially
• B-cells that divide by mitosis do not produce • it may contain antigens in the form of live or dead
antibodies and plasma cells that secrete antibodies do microorganisms, harmless (attenuated organism),
not divide toxoid (harmless toxin), surface antigens
• monoclonal antibodies – identical copies of one type
of antibody How vaccines can provide long-term immunity
1) vaccine contains antigens that stimulate an immune
1) antigen is injected into a mouse response
2) spleen cells which produce lymphocytes which 2) macrophages take up virus by phagocytosis and act
produce antibodies are removed as antigen presenting cells (APC)
3) plasma cells from spleen are fused with cancer cells 3) lymphocytes bind to these and under clonal selection
or myeloma cells forming hybridoma cells that divide 4) clonal expansion then occurs by mitosis
indefinitely 5) memory cells are formed
4) they divide by mitosis and produce antibodies 6) booster is used to further stimulate memory cell
formation

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Poor response to vaccines due to –
• suffer from malnutrition and don’t have enough
proteins to make antibodies or clones of lymphocytes
• defective immune system and don’t develop
necessary B and T cell clones

Vaccination programmes
Eradication of smallpox
• Variola virus was stable, it didn’t mutate and change
cell surface antigens
• vaccine was made from a harmless strain of a similar
virus – a ‘live’ vaccine is more effective
• infected people can be easily identified
• vaccine was freeze-dried and can be kept at high
temperatures for as long as 6 months
• didn’t affect animals – easier to break transmission
cycle

Herd immunity
Herd immunity interrupts transmission in a population so
that those who are susceptible never encounter the
infectious agents concerned.

Why measles, cholera, malaria, and TB haven’t been

eradicated
Antigenic variation
a) Antigenic drift – minor changes in the viral antigen,
memory cells are still able to recognise them and start
a secondary response

b) Antigenic shift – major changes in antigen structure

• currently there are no effective vaccines for diseases
caused by protocists as they’re eukaryotes with many
more genes.
• e.g., malaria; each stage has its own antigen

Þ measles – poor response by some children, needs

several booster shots
Þ cholera – many strains
Þ malaria – too many stages (antigenic variations)
Þ TB – symptoms may not be shown

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