IMMUNITY

NATURAL BARRIERS TO INFECTION IN HUMANS:

The body has three lines of defence to pathogens:

1. To prevent entry
2. The phagocytes gather at the site of infection where they ingest pathogens
3. The targeting of the pathogen by the specific immune response

Skin: Provides a tough physical barrier which pathogens cannot penetrate unless punctured e.g.
as a wound or cut

Hydrochloric Stomach produces HCl which kills most pathogens in our food and drink. Its low pH
acid: denatures the enzymes of the pathogens

Tears and saliva: Contain the enzyme lysozyme capable of digesting bacterial cell walls. Tears also wash
away debris and pathogens from the front of the eye.

Mucus: A sticky secretion produced by goblet cells that line the respiratory tract trap pathogens and
cilia (tiny hairs) sweep the mucus and the trapped pathogens back up the trachea

Blood clotting: Formation of a blood clot/scab which prevents pathogens entering the bloodstream
 PHAGOCYTOSIS

When pathogens do enter, phagocytosis will occur:

Phagocytosis:
- Rapid
- Carried out by white blood cells

1. Phagocyte moves towards bacterium and membrane invaginates to close the bacterium
2. Pathogen is engulfed in a phagosome
3. Lysosomes move towards the phagosome and fuses with it, releasing hydrolytic enzymes
which hydrolyse and destroy the bacterium
4. The soluble digested products are expelled from the cell by exocytosis

Antigen: Substance capable of stimulating the production of specific and complementary

antibodies; and

Antibody: Globular proteins that are specific and complementary to particular antigens that
can react with antigens leading to their destruction (details of antibody structure
and classification of antibody types not required).
 ANTIBODY-MEDIATED IMMUNITY

1. Bacteria enter the bloodstream or body fluids

2. A specific B-lymphocyte with a receptor that is complementary to the bacterial antigen
becomes sensitised or activated
3. The sensitised B-lymphocyte divides rapidly by mitosis to form a clone
4. The cloned cells develop into plasma cells and memory cells
5. Plasma cells are short lived but produce large numbers of antibodies
6. Memory cells are involved in long-term immunity and remain inactive unless stimulated by
the presence of the same antigen again

Antibodies…
… have a complementary shape to the antigens of the invading bacteria
… latch onto the bacterial antigens clumping the bacteria together
… can act as opsonins by attaching to pathogens & marking them for
phagocytosis

Agglutination:
 Immobilises the bacteria preventing its spread
 Presents a larger target for digestion by phagocytosis

Memory Cells:
 Produced by B-cells
 Long-lived (many years)
 Remain inactive until stimulated by same antigen
 Divide rapidly to produce large numbers of plasma cells and specific antibodies
 Involved in secondary immune response
 PRIMARY RESPONSE SECONDARY RESPONSE
 Slow as it takes time to activate the  Rapid as there are memory cells
specific clone and produce plasma present which are already sensitised
cells

 The individual suffers disease  Antibodies produced at a much higher

symptoms for a few days before level
antibody levels are high enough to be
effective and clear the infection

 Long-lasting as memory cells made

 CELL-MEDIATED IMMUNITY

Targets microorganisms that have non-self antigens on their surface membrane, for example:

 Macrophages/Phagocytes that have engulfed and digested a pathogen and then present
some of the foreign antigens on the cell surface membrane (known as antigen presenting
cells/APCs)
 Any type of body cell that has been invaded by a virus and then presents viral antigens on
the surface
 Abnormal self-antigens like cancer or tumour cells that are presented on the surface
 Transplanted foreign tissue antigens

T-Lymphocyte Response:

1. Viral antigen is presented on the surface of an infected cell

2. A specific T-lymphocyte with a receptor that is complementary to the viral antigen
becomes sensitised or activated
3. The sensitised T-lymphocytes divides rapidly by mitosis to form a clone
4. The cloned cells develop into killer, helper, suppressor, & memory T-cells.

T-LYMPHOCYTE ROLE IN IMMUNITY

Destroys infected cells by secreting perforin, which punches holes in the cell surface
Killer T-cell
membrane
Stimulates B-cells to divide and produce plasma cells and so increase Ab production
Helper T-cell
Activates killer T cells
Stimulates phagocytosis
Secretes interferon which limits viral replication

Do not act immediately but multiply very quickly if antigen appears again as they are
Memory T-cell
already sensitised, producing large amounts of B- and T-cells.
Provide long-term immunity

Deactivates the immune response of both B- and T-cells.

Suppressor T-cell
Important in preventing autoimmune responses
 ACTIVE & PASSIVE IMMUNITY

ACTIVE PASSIVE
Involves an individual’s own immune system
Being either natural or artificial and involving donation
producing specific antibodies, T-cells and memory
of antibodies from another source
cells to particular foreign antigens

NATURAL ARTIFICIAL NATURAL ARTIFICIAL

Infection: Vaccination: Antibodies pass naturally Antibodies which have

When Ag enters body & Dead or attenuated from mum to baby across been made in one
stimulates the immune pathogens / Modified the placenta and in the individual are injected
response to produce toxins / Isolated antigens mother’s breast milk into another person as a
antibodies serum

Individual suffers disease Long lasting Immediate protection Immediate rapid

while B- & T-cells are protection
Secondary response = Short lived
being made
more rapid & more Short lived
Long lasting antibodies
No memory cells
Secondary response = Memory cells
more rapid & more
antibodies
Memory cells
 THE IMPORTANCE OF VACCINATIONS:

To Individuals:

 Fewer people are sick, and the lives of people are extending
 World child mortality has halved in the last 25 years

To Society:

 Less people are ill, and less care is needed to tend to the ill

To the Economy:

 There are lower treatment costs to treat those who are ill
 Employees do not have to take time off work
 Carers do not have to take time off work to care for the sick

IMPORTANCE OF DISCOVERING NEW SOURCES OF ANTIBIOTICS:

To the individual & society:
 More effective treatment
 Less treatment costs
 Less time off work
 ORGAN TRANSPLANT:
The recipient’s body will try to reject the donated organ due to:
 T-lymphocytes are sensitised by the non-self antigens on the transplanted tissue cells
 T-cells cloned to produce killer T-cells
 Killer T-cells destroy transplanted cells

Successful organ transplant strategies:

 Tissue typing – Matching the donor and recipient cell surface antigen is so that there is as
good a match as possible
 Immunosuppression techniques – Drugs inhibit DNA replication and therefore the cloning of
lymphocytes, which will slow down / stop the rejection process.
 X-rays – Can be used to inhibit production of lymphocytes through the irritation of bone
marrow lymph tissue

BLOOD

Blood Group Antigens on RBC Antibodies on RBC The antibody in the

You cannot donated blood
receive a A A b doesn’t cause
foreign antigen clumping as it
in a blood B B a
becomes diluted in
transfusion the recipient’s blood
AB A+B none
O none a+b

O = Universal Donor / AB = Universal Recipient

When giving a blood transfusion, it is important that the transfusion is compatible (e.g., if
antibody a comes into contact with antigen A, then it causes the RBCs carrying antigen a to
agglutinate).
Blood agglutination can block blood capillary networks and lead to organ failure & death.
 RHESUS FACTORS & PREGNANCY
 The rhesus system is based on the presence or absence of an antigen on the cell
surface membrane of the red blood cells.
 The antigen is called the rhesus antigen or antigen D.
 If an individual possesses this antigen, they are said to be rhesus positive (Rh+).
Otherwise, they are rhesus negative (Rh-).
 There are no naturally occurring antibodies to the rhesus antigen in the blood of a
Rh- person but an immune response will be triggered if Rh+ blood is given to a Rh-
person as they will produce antibody d (anti-d).

The rhesus factor is important in childbirth when a Rh- mum has a Rh+ baby:
1. During the birth or late in pregnancy, some foetal RBCs (Rh+ so contain anti-D) leak into
the mother’s circulation
2. This causes the Rh- mother’s immune system to produce anti-D antibodies. By the time the
antibodies are produced in significant numbers by the mum, the baby will have been born
with no threat to the baby.
3. However, during subsequent pregnancies, if the foetus is Rh+ then the relevant B-
lymphocytes in the mother are already sensitised and large numbers of anti-D antibodies will
be made immediately if the foetal blood cells enter the maternal circulation. The anti-d
antibodies can cross the placenta and cause agglutination of the foetal RBCs, known as
haemolytic disease of the new-born.

To prevent this, after the birth of the first Rh+ baby, a Rh- mother is given an injection of anti-D
antibodies (i.e. passive immunity). These antibodies destroy the foetal cell fragments containing
any antigen-D before the mother can make her own antibodies actively. This means that no
memory cells are made.
If the mother becomes pregnant with a second Rh+ baby, she has never produced the memory
lymphocytes and will not pass any anti-D antibody across the placenta, so the second baby
doesn’t get haemolytic disease of the new-born. However, she will require another injection of
antibodies so she will never become sensitised to anti-D.
 ANTIBIOTIC RESISTANCE IN BACERTIA
Antimicrobial drugs can kill bacteria in 2 ways:

1. By inhibiting an enzyme involved in the formation of the cell wall of the bacteria
causing the cell to burst under osmotic pressure e.g. penicillin

2. Inhibiting metabolic processes like protein synthesis e.g. erythromycin destroys the
smaller ribosomes in bacterial cells

Antibiotic resistance is an example of directional selection

Factors which have led to an increase in antibiotics resistance
1. Over prescription of antibiotics that the body could naturally fend off
2. Patients not completing a course of antibiotics
3. Poor drug quality – in some parts of the world drug production is poor and drugs are
stockpiled and not used for a long time
4. Urbanisation – more people living in close proximity
5. Global trade and travel make it easier for disease to spread
6. Use of antimicrobials in veterinary medicine

Steps put in place by hospitals to reduce the spread of infection:

- A more vigorous hygiene culture
- Effective isolation of MRSA patients
- A reduction in the prescription of antibiotics
 FACTORS AFFECTING DISEASE SPREAD:

1. How easily it is spread from person to person

2. How likely for the infected person to get sick
3. If there is a vaccination for the disease
4. Percentage uptake for that vaccination
5. Is there a bacterial resistance to the disease

Epidemic: Disease which spread through a small region and affect a large proportion of the
population
Pandemic: An epidermic that has spread worldwide. A global disease outbreak affecting
many thousands of people over several countries at the same time.

Most epidemics and pandemics are caused by viruses

 Viruses have very small genomes which are prone to mutations
 Many viruses that cause disease are retroviruses with RNA genomes which are much less
stable than DNA
 Antibiotics are not effective against viruses
 Some may become airborne
 ANIMALS AS RESERVOIRS OF DISEASE-CAUSING VIRUSES

Zoonotic Disease: A disease which is transferred from animals to humans

Zoonotic diseases can spread in many ways:

1. Working closely with livestock
2. Contact with pets, exhibited animals or wildlife
3. Contact with soil or water contaminated by animals
4. Consumption of unpasteurised dairy products

Bats are good reservoirs because:

1. They are mammals and have a similar physiology to humans
2. Live in large colonies so spread virus easily
3. Fly large distances and so easily spread disease
4. Can carry disease without suffering symptoms themselves
5. Long lifespan

There is an increase in zoonotic diseases due to a loss of habitats for bats (urbanisation, clearing
of woodland etc.), so bats are forced into areas where they live in closer proximity to humans.
 DIAGNOSING INFECTION – ELISA
ELISA is a laboratory technique that uses enzymes, antibodies, and antigens to detect and
quantify substances (e.g. proteins, hormones) in body fluids which can be indicators of disease

Method:
1. Body fluids from a patient are added to 96-well plate
2. Antibodies are added to these wells
3. A reaction between antibody and antigen triggers an enzyme linked to the antibody,
causing a colour change
4. Antigens can then be identified

ELISA diagnostics kit used to detect:

 Pathogens in the body
 Cancer cell markers
 Cardiac disease markers
 Pregnancy tests

Advantages:
 Early, rapid screening
 Can screen for a number of conditions at the same time