1. Antibody production and vaccination
Immunity is based on recognition of self and destruction of foreign material.
AHL Topic 11.1
IB Biology
Miss Werba

2. TOPIC 11 – ANIMAL PHYSIOLOGY
11.1
ANTIBODY PRODUCTION & VACCINATION
11.2
MOVEMENT
11.3
THE KIDNEY & OSMO-REGULATION
11.4
SEXUAL REPRODUCTION
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3. THINGS TO COVER Statement Guidance U.1 U.2 U.3 U.4 U.5 U.6 U.7 U.8 U.9
Every organism has unique molecules on the surface of its cells.
U.2
Pathogens can be species-specific although others can cross species barriers.
U.3
B lymphocytes are activated by T lymphocytes in mammals.
U.4
Activated B cells multiply to form clones of plasma cells and memory cells.
U.5
Plasma cells secrete antibodies.
U.6
Antibodies aid the destruction of pathogens.
U.7
White cells release histamine in response to allergens.
U.8
Histamines cause allergic symptoms.
U.9
Immunity depends upon the persistence of memory cells.
U.10
Vaccines contain antigens that trigger immunity but do not cause the disease.
U.11
Fusion of a tumour cell with an antibody-producing plasma cell creates a hybridoma cell.
U.12
Monoclonal antibodies are produced by hybridoma cells.
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4. THINGS TO COVER Statement Guidance A.1 A.2 A.3 S.1 NOS 4.5
Smallpox was the first infectious disease of humans to have been eradicated by vaccination.
A.2
Monoclonal antibodies to HCG are used in pregnancy test kits.
A.3
Antigens on the surface of red blood cells stimulate antibody production in a person with a different blood group.
S.1
Analysis of epidemiological data related to vaccination programmes.
NOS 4.5
Consider ethical implications of research— Jenner tested his vaccine for smallpox on a child.
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5. CELL SURFACE MARKERS
U.1
Every organism has unique molecules on the surface of its cells.
These molecules have a wide range of functions.
An MHC marker labels the body’s cells as “self”.
An antigen is a molecule that the immune system recognises as “non-self”.
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6. REVISION: ABO BLOOD GROUPING
TOPIC 3.4 – A.1
ABO blood type is controlled by multiple alleles coding for different antigens on red blood cells
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7. ABO BLOOD GROUPING
A.3
Antigens on the surface of RBCs stimulate antibody production in a person with a different blood group.
These antigens are called agglutinogens.
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8. ABO BLOOD GROUPING
A.3
Blood type O is the universal donor, as it has no antigens that the recipient’s immune system can react to.
Blood type AB is the universal recipient.
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9. REVISION 1st line of defence: 2nd line of defence:
TOPIC 6.3
1st line of defence:
unbroken skin, mucous secretions, body secretions, gut
2nd line of defence:
Inflammation  increases blood flow
Non-specific cellular response  platelets, leucocytes
Fever  kills pathogens; increases activity of IS
Protein responses  complement, interferon
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10. REVISION 3rd line of defence: Involves the immune response
TOPIC 6.3
3rd line of defence:
Involves the immune response
Antigen presentation
Activation of Helper T cells
Activation of B cells
Production of plasma cells
Production of memory cells
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11. REVISION
TOPIC 6.3
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12. Antigen presentation by macrophage
REVISION
TOPIC 6.3
Pathogen invades the body.
The pathogen’s antigen detected as “non-self” by macrophages.
Macrophage tries to ingest the pathogen (phagocytosis) but the ingestion isn’t complete.
Macrophage displays the bacterial antigen on its own cell membrane.
Macrophage has become an antigen presenting cell (APC).
Antigen presentation by macrophage
MHC II protein
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13. REVISION The APC comes into contact with lymphocytes.
TOPIC 6.3
The APC comes into contact with lymphocytes.
A Helper T (TH) cell complementary to the antigen on the APC will be identified.
Selected TH cell divides by mitosis forming a clone.
These processes are known as clonal selection & clonal expansion.
Memory T cells are also formed.
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14. REVISION Inactive Helper T-cell
TOPIC 6.3
Inactive Helper T-cell
Macrophage sends a signal to activate the helper T-cell
Active Helper T-cell
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15. REVISION
TOPIC 6.3
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16. B CELL ACTIVATION The TH cells activate complementary B cells
U.3
The TH cells activate complementary B cells
The B cells also divide to form a clone.
Helper T cell presents antigen to B cells
Activates complementary B cell
B cell divides
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17. B CELL ACTIVATION B CELL ACTIVATION: Active Helper T-cell Antibody
U.3
B CELL ACTIVATION:
Active Helper T-cell
Antibody
Activated Helper T-cell sends a signal to activate the B-cell
Activated Helper T-cell binds to B-cell
Inactive B-cell
Active B-cell
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18. PLASMA CELL ACTIVATION
U.3
U.5
U.6
Activated B cells differentiate into plasma cells.
Plasma cells make large numbers of antibody proteins.
The antibodies are secreted by exocytosis.
 aid destruction of pathogen
Differentiation of B cell
Plasma cell formation
Antibody production
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19. MEMORY CELL ACTIVATION
U.3
U.5
Activated B cells also differentiate into memory B cells.
Memory cells remain after immune response.
Allow a rapid response if the disease is encountered again (=LONG TERM IMMUNITY)
Differentiation of B cell
Plasma cell formation
Antibody production
Memory B cell formation
Long term immunity
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20. 11.1.2
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21. IMMUNE RESPONSE
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22. ANTIBODY PRODUCTION
U.6
Antibodies (immunoglobulins): proteins produced as a response to the presence of an antigen
General structure of an antibody:
2 antigen-binding sites
MHC proteins (major histocompatibility complex)
T cell receptors do not respond to antigens unless the antigens are associated with MHC proteins
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23. ANTIBODY PRODUCTION
U.6
The antibodies produced by a plasma cell are complementary to the original antigen presented on the pathogen.
They aid the destruction of pathogens.
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24. ANTIBODY PRODUCTION
U.6
What happens after the antibody has bound to the antigen?
Enhances phagocytosis
Leads to cell lysis
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25. ANTIBODY PRODUCTION
U.6
Neutralisation – attachment of Abs stops toxins from affecting or entering cells, viruses from invading cells, etc
Opsonisation – Abs attach to pathogens, marking them for destruction by immune cells – eg. macrophages
Agglutination – Abs attach to each other causing the pathogens to clump together, enhancing opsonisation and neutralisation.
Complement activation – Abs encourage other components to attack the pathogen and lyse the cell
Inflammation – Abs can also cause localised inflammation to help combat the pathogen
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26. HISTAMINE Histamine is produced by 2 types of leukocytes (WBCs):
Basophils
Mast cells
Mast cells are found in connective tissues.
If they are triggered by an infection, they release histamine into the area.
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27. HISTAMINE
U.7
U.8
Histamine increases the permeability of the capillaries to WBCs and some proteins (eg. antibodies).
This will allow the immune system components to engage the pathogen at the site of infection.
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28. HISTAMINE
U.7
U.8
Some mast cells can become sensitised by binding of an antibody (IgE).
Some environmental chemicals called allergens (eg. pollen) can cause these mast cells to release large quantities of histamine.
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29. IMMUNITY
U.10
Immunity: having sufficient biological defences against infection
Active immunity: immunity due to the production of antibodies by the organism itself after the immune response has been stimulated by a pathogen
Passive immunity: immunity due to acquisition of antibodies from another organism in which active immunity has been stimulated
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30. IMMUNITY Acquired immunity Naturally acquired Active Passive
Infection; contact with pathogen
eg. chicken pox immunity
Passive
Antibodies pass from mother to baby
eg. via placenta & colostrum
Artificially acquired
Vaccine; dead or attenuated pathogens eg. MMR vaccine
Injection of antiserum (antibodies) eg. rabies treatment
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31. IMMUNITY
U.9
U.10
The secondary response to an antigen is much faster and stronger than the first response.
Vaccinations deliberately expose someone to a disease so that they develop immunity – without them having to contract the illness itself.
Vaccines contain a form of the pathogen or toxin that has been modified (attenuated) so that it is unable to harm the body.
Exposure to an attenuated pathogen still allows the production of memory cells against the antigen.
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32. IMMUNITY
U.9
U.10
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33. SMALLPOX Caused by the variola virus
First infectious disease of humans to be eradicated by vaccination in 1980.
Achieved worldwide!
Last known case was in
Other eradication programs have been less successful, but have reduced numbers.
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34. JENNER’S RESEARCH Consider the ethical implications of research
NOS 4.5
Consider the ethical implications of research
Jenner tested his vaccine for smallpox on a child.
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35. JENNER’S RESEARCH
A.1
Edward Jenner used cowpox (a virus similar to smallpox) when he was trying to develop the smallpox vaccine
In 1796, he deliberately infected an 8y.o. boy with cowpox.
Then he deliberately infected the boy with smallpox, but he found that the boy was immune.
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36. JENNER’S RESEARCH Ethical issues:
No prior research into human testing & side- effects of cowpox
No informed consent
Child too young to understand dangers and provide informed consent anyway
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37. SPECIES-SPECIFIC PATHOGENS
U.2
Many pathogens are species-specific:
eg. polio, measles, syphillis
Others (75%) are zoonotic – meaning that they can be transmitted between humans and other animals:
eg. flu, ebola, salmonella
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38. MONOCLONAL ANTIBODIES
U.11
U.12
Antibodies can be produced in a lab for therapeutic or diagnostic use.
Monoclonal antibodies are derived from a single cell.
They are pure antibody preparations that are specific for a single antigen.
The current technology for making monoclonal antibodies involves fusion of tumour cells and B cells.
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39. MONOCLONAL ANTIBODIES
U.11
U.12
PRODUCTION:
A mammal (eg. mouse) is injected with the antigen.
The mouse plasma cells will produce antibodies against the antigen.
The mouse plasma cells complementary to the antigen are extracted and fused with tumour cells  forms a hybridoma cell
The hybridoma cell divides and produces identical antibodies to the original plasma cell.
The antibody can then be harvested.
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40. MONOCLONAL ANTIBODIES
U.11
U.12
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41. MONOCLONAL ANTIBODIES
USES:
Pregnancy testing
detects the presence of the HCG hormone in the urine
HCG is only released during pregnancy
Testing for a suspected heart attack
Damaged heart muscle cells release a specific cardiac enzyme into the blood
ELISA test for HIV
Colour change in dimple tray when antibodies are detected
Treatment for rabies
Diagnosis of malaria
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42. MONOCLONAL ANTIBODIES
U.11
U.12
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43. EPIDEMIOLOGY
S.1
Epidemiology: the study of the incidence, distribution and control of diseases
Analysing epidemiological data can help guide vaccination programs:
Early detection of outbreaks
Analysis of transmission
Can get more accurate data than the estimates
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44. EPIDEMIOLOGY
S.1
eg. measles vaccine
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45. EPIDEMIOLOGY eg. measles vaccine
◼Africa ◼Eastern Mediterranean ◼South-East Asia
◼Americas ◼Europe ◼Western Pacific
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46. ANTIBODY PRODUCTION & VACCINATION
Q1.
Using the diagram, outline the annual pattern in the data seen across all regions.
Identify the regions impacted most greatly by outbreaks.
Since 2010, identify the regions in which the incidence of measles is: i. decreasing ii. increasing
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47. ANTIBODY PRODUCTION & VACCINATION
Q1.
Despite having an established vaccination programme in most countries, Europe has seen a peak in measles incidence between 2010 and Suggest a reason for this (Try researching it!).
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48. ANTIBODY PRODUCTION & VACCINATION
Q2. What are fused in the production of monoclonal antibodies?
Tumour cells and T cells
Tumour cells and B cells
B cells and T cells
Antibodies and antigens
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49. ANTIBODY PRODUCTION & VACCINATION
Q3. State one use of monoclonal antibodies in diagnosis and one use in treatment. [2] Q4. Outline the principle of immunity. [6] Q5. AHL version - Explain the production of antibodies. [7]
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