1. starter CELL comparison Cell Natural Killer Cell B Lymphocyte
T Lymphocyte
Part of immune system
Specific made in bone marrow
Types? / Subspecies?
N/A
Works on
Virus/ cancer cells
Support other cells
Mode of action?
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2. starter CELL comparison Cell Natural Killer Cell B Lymphocyte
T Lymphocyte
Part of immune system
Non-specific
Specific made in bone marrow
Specific made in thymus
Types? / Subspecies?
N/A
Activated plasma cell or memory B cell
Cytotoxic or helper T cells
Works on
Virus/ cancer cells
External pathogen
Support other cells
Mode of action?
Perforins, signal molecules switch on genes which make degradative enzymes triggering cell apoptosis
Clonal selection of 1 specific antibody receptor, proliferate and make antibodies, trap/neutralise for phagocytes or cause cell lysis. Memory cells remain for subsequent attack.
Clonal selection, helper T cells produce cytokines for other cells to be activated. Killer cells see antigen, then clonally selected and can induce apoptosis. Memory cells remain for subsequent attack.
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3. Big picture Immune system diseases Non specific immunity
Disease survival mechanisms
Physical & chemical barriers
Infectious Disease
Inflammatory
Transmission
Epidemiology
Non-specific Cellular response
Specific immunity
Vaccination
Public Health
Immunological surveillance
B cells
T cells
Clonal Selection theory
Memory cells
Big picture

4. Learning outcomes Recap clonal selection theory
Explain importance of antigen presenting cells in the activation of cells
Use the pattern of the response curve to demonstrate the importance of Memory cells

5. Clonal selection theory
The body has a large number of lymphocytes each with a single type of membrane receptor specific for one antigen.
When a receptor is activated by the binding of an antigen, the lymphocyte repeatedly divides resulting in a clonal population of lymphocytes.
To become fully activated – antigen presenting cells are needed
Cell division

7. Antigen presenting cells
Ingested pathogens (phagocytes like macrophages) or infected cells display fragments of the pathogen on the surface of the cell
These , research have shown, are playing an ever increasing role in the immune system, as they activate other cells.

8. Memory cells
Some T and B lymphocytes produced in response to antigens by clonal selection survive long term as memory cells.
A secondary exposure to the same antigen rapidly gives rise to a new clone of lymphocytes producing a rapid and greater immunological response.

9. Primary .vs. Secondary Immune Response
Primary Immune Response
This is a response to an invader the First time the invader infects the body.
No measurable immune response for first few days.
Next 10 – 15 days antibody production grows steadily
Secondary Immune Response
A more rapid response to an invader the 2nd time it invades the body.
Antibody production increases dramatically and in a much shorter time period..

10. Primary .vs. Secondary Immune Response

11. Demonstrate your understanding
You will be given 9 statements and a graph.
You must put the statements in order and write them on the graph
Do not cut the statements out

12. Primary – establishes immunological
memory

13. Primary and secondary responses
Annotate your graph of the primary and secondary responses by adding the following labels:
First dose of antigen
Second dose of antigen
Time between 1st and second exposure
Primary response
Secondary response
Questions:
Compare the primary and secondary responses in terms of time taken, decline of antibodies and antibodies produced.
Memory cells are produced in the primary response, how else could these be produced without the person being infected?
Extra challenge: What causes the secondary response to occur more rapidly?
LO:

14. Antibody Concentration – Primary and Secondary Response
Primary Response
Infection (Ag)
Lag phase
3 Antibodies produced
4 Antibody level rises
to combat infection
5 Ag dealt with
6 Ab level declines – short lived
Secondary Response
After the primary response, Ab’s do not stay in blood – the level declines
If the body is infected by the same Ag a second time Ab’s must be made again
Re-infection causes much more rapid and a stronger immune response – concentration of Ab’s rises sooner- reaches a higher concentration – more plasma cells than in 1o response – more cells to respond to Ag; less time to produce same number of plasma cells –hence, a greater [Ab] compared to 1o response; increased affinity of Ab for Ag.
This is due to the presence of memory cells (made during the primary response) – no need for antigen presentation and clonal selection
Long-lived; basis of vaccination

15. Concentration of anti-Rubella antibody in the blood/arbitrary units
The graph below shows the levels of anti-Rubella (German Measles) in the blood B
Secondary Response 10 20 30
100
1000
10000 A
Primary Response
Concentration of anti-Rubella antibody in the blood/arbitrary units
Long interval
First exposure to antigen X
Second exposure to antigen Y
Time/days
infection, or
vaccination

16. Concentration of anti-Rubella antibody in the blood/arbitrary units
The graph below shows the immune response of two mice exposed to a pathogen. Both mice were expose on day 0 of the experiment
Mouse A
Mouse A
10000
1000
Concentration of anti-Rubella antibody in the blood/arbitrary units
100 10 10 15 20 25 5
Time/days

17. Plenary: True or False? Antibodies are produced by memory cells.
Antibodies can detect any antigen.
A antigen-antibody complex is formed when an antibody binds to a pathogen’s antigens.
Agglutination makes it easier for phagocytes to engulf pathogens.
Neutralisation only occurs with viruses.
Opsonisation causes phagocytes to swell and burst.
Antibodies can stop viruses entering host cells.
The primary immune response produces memory cells.
The secondary immune response is caused by vaccination.
The secondary immune response is quicker.

18. Summary slide Specific defences Immune surveillance
A range of white blood cells constantly circulate monitoring the tissues.
If tissues become damaged or invaded, cells release cytokines which increase blood flow resulting in specific white blood cells accumulating at the site of infection or tissue damage.
Recognition of self and non self through specific surface proteins (antigens)
Lymphocytes respond specifically to antigens on foreign cells, cells infected by pathogens and toxins released by pathogens.

19. Summary slide specific defences Clonal selection theory
The body has a large number of lymphocytes each with a single type of membrane receptor specific for one antigen.
When a receptor is activated by the binding of an antigen, the lymphocyte repeatedly divides resulting in a clonal population of lymphocytes.

20. Summary slide Specific defences Immunological memory cells
Some T and B lymphocytes produced in response to antigens by clonal selection survive long term as memory cells.
A secondary exposure to the same antigen rapidly gives rise to a new clone of lymphocytes producing a rapid and greater immunological response.