Chapter 24 – Body defence mechanisms

Name: ___________________________ Class: __________( )

A. Non-specific defence mechanisms B. Specific defence mechanisms

1. Physical barriers & chemical barriers 1. Humoral immune response (HIR) 5. Active immunity & passive
2. Blood clotting 2. Cell-mediated immune response (CMIR) immunity
3. Phagocytosis 3. Primary response & secondary response
4. Inflammatory response 4. Vaccination

Body defence
mechanisms

Non-specific
Specific defence
defence
mechanisms
mechanisms

Cell-mediated
Physical & Inflammatory Humoral immune
Blood clotting Phagocytosis immune response
chemical barriers responses repsonse of B cells
of T cells

1st line of defence 2nd line of defence 3rd line of defence

A. Non-specific defence mechanisms

1. Physical barriers & chemical barriers (p.3-4)

Physical barriers
- mechanical block
 prevent entry of
pathogens
Chemical barriers
- secretions that kill
or inhibit the growth
of pathogens
 prevent entry of
pathogens

i. Physical barrier (p.3-4)

Skin (p.3)
- covers almost the whole body
- outermost layer of epidermis made of dead cells
 form a tough and impermeable layer
 prevent entry of pathogens

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Chapter 24 – Body defence mechanisms

Inner surface of respiratory tract (p.4) DSE2014 (modified):

i. Name cells A and B

 A: ciliated epithelial cell B: mucus-secreting cell

ii. With reference to the features of the inner wall shown in the photomicrograph, describe how the inner wall of the
trachea can protect our body against bacterial invasion. (3)

 mucus secreting cells secrete mucus to trap germs / pathogens / bacteria / microbes from the incoming air
 cilia sweep the trapped germs away to the throat for swallowing or coughing
 closely packed epithelial cells prevent the entry of bacteria / form a physical barrier

ii. Chemical barrier (p.4)

Tears Saliva
- secreted by tear gland - secreted by salivary
 contain lysozyme gland
 kill bacteria  contain lysozyme
 kill bacteria

Sebum Gastric juice

- secreted by sebaceous - secreted by gastric gland
gland  contain hydrochloric
 kill pathogens on skin acid
 kill bacteria in food

Vaginal secretion
- acidic
 inhibit bacterial growth

CE2000: In the alimentary canal, bacteria in food are mainly killed by

A. saliva. B. mucus.
C. gastric juice. D. pancreatic juice.

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Chapter 24 – Body defence mechanisms

DSE2012 Practice: Which of the following parts of the human skin are responsible for preventing us from microbial
infections?
(1) sebaceous gland
(2) epidermis
(3) hair

A. (1) and (2) only B. (1) and (3) only

C. (2) and (3) only D. (1), (2) and (3)

2. Blood clotting (p.3)

i. Formation of blood clot

1. blood platelets start off a series of reactions
2. soluble fibrinogen is converted to insoluble fibrin
 form a net
3. blood platelets, red blood cells and white blood cells are
trapped in the net
 blood clot formed

ii. Importance of blood clotting

- prevents further bleeding
- seals the wound and form a physical barrier to prevent the
entry of pathogens
- protects the injured tissue

CE2009: Which of the following components of blood helps to prevent the entry of pathogens into the human body?

A. blood platelets B. lymphocytes C. phagocytes D. antibodies

DSE2015: Which of the following components of blood are involved in forming a blood clot?
(1) Blood platelets
(2) Red blood cells
(3) White blood cells

A. (1) and (2) only B. (1) and (3) only C. (2) and (3) only D. (1), (2) and (3)

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Chapter 24 – Body defence mechanisms

3. Phagocytosis (p.5)
1. phagocytes engulf the pathogens by phagocytosis
2. pathogens are digested by enzymes
3. waste materials are released

 certain kind of phagocytes present the antigen of

pathogens to lymphocytes to trigger immune response
[p.5-6]

Q: In relation to the function of phagocytes, which two types of organelles are abundant in phagocytes?

 They contain a lot of rough endoplasmic reticulum

 for the synthesis of enzymes.
 They also contain a lot of mitochondria
 to provide energy for the synthesis of enzymes.

4. Inflammatory response (p.6)

i. Process
1. damaged cells release chemical signals (e.g.
pathogen Hotness histamine)
2. arterioles dilate
 blood flow increases
3. permeability of capillaries increases
 more phagocytes can pass through and
reach the wound to kill the pathogens
- pus may form
 killed pathogens
dead white blood cells
2 3 capillaries lack muscular wall
ii. Symptoms and cannot dilate
- Redness - Swelling
 dilation of arterioles  increased blood flow to injured tissues & increased permeability of
 blood flow to injured tissues increases capillary
 increased formation of tissue fluid
- Hotness
 accumulation of tissue fluid
 dilation of arterioles
 blood flow to injured tissues increases - Pain
 more tissue fluid accumulates and build up pressure
 presses against nerve endings
 stimulate the pain receptors in the skin

DSE2012: After injury, the wound usually becomes swollen due to

A. accumulation of bacteria at the wound. B. accumulation of tissue fluid at the wound.
C. increased phagocytosis at the wound. D. increased blood flow to the capillaries around the wound.

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Chapter 24 – Body defence mechanisms

B. Specific defence mechanisms

1. Humoral immune response (HIR) (p.10-11)
i. Process (p.10) [primary response p.6-7]
1. foreign antigens bind to the receptors of B cells
2. B cells are stimulated to multiply and differentiate into
plasma cells and memory B cells
 plasma cells produce antibodies against pathogens
with that antigen
 memory B cells develop memory for secondary
response [p.6-7]

ii. Adaptive features of plasma cell (p.10)

With reference to the diagram on the left, explain how plasma cell is
adapted to its function. (4)

 A large number of rough endoplasmic reticulum

 for the synthesis of antibodies

 A large number of mitochondria

 provides energy for the synthesis of antibodies

iii. Actions of antibodies (p.11)

- The action of antibodies is specific against a specific
antigen
 the shape of antigen binding site can only fit certain
antigens

Three ways of actions

- Agglutination - Neutralization - Lysis
 antibodies clump the  antibodies bind to toxins and act as  antibodies bind to antigen
pathogens together antitoxins to neutralize them  attracts certain proteins in blood
 facilitate phagocytosis  facilitate phagocytosis to form pores on cell membrane
antigen

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Chapter 24 – Body defence mechanisms

2. Cell-mediated immune response (CMIR) (p.12)

i. Process [primary response p.6-7]
1. foreign antigens bind to the receptors
of helper T cells
2. helper T cells secretes lymphokines
stimulate T cells to multiply and
differentiate into killer T cells and
memory T cells
 killer T cells directly kill infected cells
 memory T cells develop memory for
secondary response [p.6-7]
also kill cancer cells

3. Primary response & secondary response (p.15)

i. Primary response (p.15) [HIR p.5] ii. Secdonary response (p.15) [CMIR p.6]
- first exposure to an antigen - secondary exposure to the same antigen
- it takes time for B cells to multiply and differentiate into - memory cells recognize the antigen
plasma cells and memory B cells / T cells to multiply and - memory cells multiply and differentiate into a larger
differentiate into killer T cells and memory T cells number of plasma cells, killer T cells and memory cells in
 slow a shorter time
 latent period before the rise in antibody level - larger amount of antibodies are produced in a shorter
time
 faster, stronger & longer lasting than primary

memorization tools response

- Primary response of B cells - Secondary response of B cells

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Chapter 24 – Body defence mechanisms

- Primary response of T cells - Secondary response of T cells

Q: Explain why the change in antibodies level in blood in secondary response is faster and stronger than that in
primary response. (4)

 Memory B cells for the antigen is produced in the primary response.

 In the secondary exposure, the same antigen is recognized by the memory B cells produced in the primary
response.
 Memory B cells multiply and differentiate quickly into larger amount of plasma cell and memory B cell.
 Plasma cells produce larger amount of antibodies in a shorter time.

iii. Flow chart of primary & secondary immune responses (p.22)

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Chapter 24 – Body defence mechanisms
Practice
CE1999: Which of the following statements about antibodies is incorrect?

A. They are proteins. B. They can kill bacteria.

C. They are specific in action. D. They have a memory of the bacteria

CE1994: i. The increase in the antibody concentration on day 7 might be

caused by

A. excessive bleeding.
B. the entry of bacteria.
C. recovery from a disease.
D. the intake of a large amount of antibiotics.

ii. The antibody concentration increased rapidly on day 21 because

the person

A. developed a fever.
B. received a vaccination.
C. was infected by the same type of antigen.
D. produced a large number of phagocytes.

DSE2012 Sample:

Which of the following graphs best represents the changes in concentration of antibody in the blood?

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Chapter 24 – Body defence mechanisms

4. Vaccination (p.16-17)
i. Principle (p.16)
- introduction of antigen into body
 stimulate primary response of B cells & T cells
 produce memory cells for that antigen
 produce secondary response in subsequent
invasion by the same antigen
 prevention of diseases

- booster doses
 stimulate the production of more memory cells
and antibodies
 maintain immunity (protection from diseases)

ii. Antigens in vaccines (p.16)

- live, weakened pathogens - subunits of pathogens, e.g. viral proteins
- killed pathogens - inactivated bacterial toxins

- mRNA vaccines
- injection of mRNA encoding viral
proteins (e.g. surface proteins)
- ribosomes in our body translate the
mRNA and synthesize the viral proteins
(antigen) [Ch.26]

iii. Blood test of antigens and antibodies (p.17)

DSE2015 (modified): The results of blood tests for the presence of antigens and antibodies of hepatitis B in four
individuals:
Individual 1 Individual 2 Individual 3 Individual 4
Antigens of hepatitis B Negative Positive Negative Positive
Antibodies of hepatitis B Negative Negative Positive Positive

i. Which individuals have contracted hepatitis B? ii. Which individual(s) would you recommend for vaccination
against hepatitis B?
A. 1 and 3 only B. 2 and 4 only
C. 3 and 4 only D. 2, 3 and 4 A. 1 only B. 4 only
C. 1 and 2 only D. 1 and 3 only

iv. Invention of vaccine (p.17)

- infection of cowpox (mild) provides protection from
smallpox (lethal)
∵ similar antigens of the two viruses
 memory cells for cowpox can recognize smallpox
 produce secondary response

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Chapter 24 – Body defence mechanisms

4. Active immunity & passive immunity (p.20)

Injection of
antibodies
i. Active immunity
- antibodies produced by our own body
during immune response
- antigens needed
 memory cells produced
 slow but long lasting
e.g. recovery from infection, vaccination

ii. Passive immunity

- antibodies acquired by direct transfer
from immune individuals immunity  protection from diseases
- antigens not needed
 fast but short lived
∵ no memory cells produced; unused
antibodies will be broken down
e.g. transfer of maternal antibodies
through placenta / breastfeeding, injection
of antibodies (e.g. serum)

CE2000 i. Substance P can be

(1) bacteria.
(2) antigens.
(3) antibodies.

A. (1) only
B. (3) only
C. (1) and (2) only
D. (2) and (3) only
ii. What is the advantage of method 2 over method 1 in inducing immunity?

A. The immunity can last longer.

B. The immunity can develop faster.
C. It can stimulate the white blood cells to produce more antibodies.
D. The body can become immune against a wider range of disease.

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