Cambridge International AS & A Level Biology 9700: Immunity – Revision Notes

For full explanations and a worked data example, use the immunity study guide. These notes condense topic 11 of the Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027: section 11.1 The immune system (outcomes 1–4) and section 11.2 Antibodies and vaccination (outcomes 1–6). It is AS Level content, examined on Papers 1 and 2, and Paper 4 can draw on it too. Every outcome applies to all candidates.

Links: Cambridge AS & A Level Biology hub, printable checklist, practice questions for this topic, 9700 AS diagnostic and the previous topic, infectious diseases revision notes.

Key definitions

Term	What to write
Antigen	A molecule (usually a protein or glycoprotein) that is recognised by the immune system and stimulates an immune response
Self antigen	An antigen on your own cells; does not normally trigger a response
Non-self antigen	A foreign antigen (on a pathogen, transplant or mismatched blood) that triggers a response
Antibody	A glycoprotein secreted by a plasma cell that binds specifically to one antigen
Clonal selection	Only lymphocytes with receptors complementary to the antigen are activated
Clonal expansion	The selected lymphocytes divide by mitosis to form a clone
Monoclonal antibody	Many identical antibodies of one type, made by a clone of hybridoma cells
Vaccine	A preparation containing antigens that stimulates an immune response to give long-term immunity
Herd immunity	Protection of a population, including unvaccinated people, because so many are immune that transmission breaks down

11.1 The immune system

Phagocytes (non-specific)

Neutrophils	Macrophages
Lobed nucleus	Large, rounded nucleus
Many in blood; first to arrive	Monocytes in blood settle in tissues as macrophages
Short-lived	Long-lived
Engulf and digest	Engulf, digest and present antigens to lymphocytes

Phagocytosis in steps: chemotaxis → receptors bind the pathogen → membrane engulfs it (endocytosis) → phagocytic vacuole → lysosomes fuse and release hydrolytic enzymes → pathogen digested.

Lymphocytes (specific)

Cell	Role in the response
Macrophage	Engulfs pathogen; displays its antigens (antigen-presenting cell)
T-helper cell	Binds presented antigen; divides; releases cytokines that activate B-cells and T-killer cells
T-killer cell	Binds to infected body cells showing the antigen and kills them
B-lymphocyte	Selected by antigen; divides; forms plasma cells and memory B-cells
Plasma cell	Lots of rough ER and Golgi; secretes antibodies
Memory cell (B and T)	Long-lived; remains after infection; gives the secondary response

Primary response in steps

1. Macrophage engulfs the pathogen and presents its antigen.
2. Matching T-helper cell binds (clonal selection).
3. T-helper cells divide by mitosis and release cytokines.
4. Cytokines stimulate matching B-cells and T-killer cells to divide (clonal expansion).
5. B-cells become plasma cells (antibodies) and memory cells.
6. T-killer cells destroy infected cells; some T-cells become memory cells.

Primary vs secondary response

	Primary	Secondary
Trigger	First exposure to antigen	Later exposure to the same antigen
Cells responding	Few matching lymphocytes	Many memory cells
Delay before antibody rises	Several days	Short
Peak antibody concentration	Low	Much higher
Symptoms	Usually	Usually none: pathogen destroyed first

11.2 Antibodies and vaccination

Antibody structure → function

• 2 heavy + 2 light polypeptide chains, joined by disulfide bonds → stable Y shape (quaternary structure).
• Variable region → antigen-binding site with a shape complementary to one antigen.
• Two binding sites → agglutination (clumping pathogens).
• Hinge region → flexibility to bind two antigens different distances apart.
• Constant region → binds receptors on phagocytes.
• Also: neutralise toxins; block the sites viruses use to enter cells.

Hybridoma method in steps

1. Inject mouse with antigen.
2. Remove antibody-making B-lymphocytes from its spleen.
3. Fuse with myeloma (cancer) cells → hybridoma cells.
4. Select the hybridoma that makes the required antibody.
5. Clone it in culture; collect the monoclonal antibody.

Why fuse? Plasma cells make the antibody but cannot divide; myeloma cells divide indefinitely.

Monoclonal antibodies: principles of use

Use	Principle
Diagnosis	Antibody carries a marker (fluorescent, radioactive or coloured) and binds only where its antigen is: locates cancers or clots, detects pathogens or hormones (e.g. hCG in pregnancy tests)
Treatment	Antibody binds a specific antigen on target cells: blocks a receptor, marks cells for destruction, or delivers an attached drug or toxin only to those cells
Problem	Mouse antibodies are non-self in humans, so they are “humanised” to reduce an immune response against them

Four types of immunity

	Natural	Artificial
Active: own antibodies, memory cells, long-term	Having an infection	Vaccination
Passive: antibodies from outside, no memory cells, short-term	Across the placenta; in breast milk	Injection of ready-made antibodies

Vaccines and programmes

• Vaccines contain antigens: live attenuated, killed or inactivated pathogens, toxoids, or isolated antigens.
• They cause a primary response without disease → memory cells → long-term (artificial active) immunity. Boosters increase memory cell numbers.
• Programmes give herd immunity and allow ring vaccination around new cases.
• Harder when: antigens change (antigenic variation) or there are many strains; the pathogen hides inside cells; people are malnourished or immunosuppressed; vaccines need cold storage; uptake is low.

Must-know distinctions

• Antigen vs antibody: the antigen is the molecule recognised; the antibody is the protein made to bind it.
• Specific vs non-specific: lymphocytes respond to one antigen; phagocytes engulf any pathogen.
• T-helper vs T-killer: helpers release cytokines; killers destroy infected cells. Neither makes antibodies.
• Plasma cell vs memory cell: plasma cells secrete antibody and are short-lived; memory cells last for years and do not secrete antibody until activated.
• Active vs passive: made by you (with memory) vs given to you (no memory).
• Natural vs artificial: occurs in normal life vs given deliberately by medical intervention.
• Vaccine vs antibody injection: a vaccine gives antigens (active); an antibody injection gives passive immunity.

Quick self-test

1. State two differences between neutrophils and macrophages.
2. Name the organelles that fuse with a phagocytic vacuole and state what they release.
3. Explain what is meant by a non-self antigen.
4. Explain why only a few B-lymphocytes respond to a particular pathogen.
5. State the role of cytokines in the primary response.
6. Suggest why plasma cells contain a lot of rough endoplasmic reticulum.
7. Explain why a second infection by the same strain of a pathogen usually causes no symptoms.
8. State how the structure of the variable region allows an antibody to be specific.
9. Explain why plasma cells are fused with myeloma cells in the hybridoma method.
10. A traveller is injected with ready-made antibodies before a trip. State the type of immunity and explain why it lasts only a short time.
11. Suggest why it has been difficult to produce an effective vaccine against HIV.
12. In a district, 11 280 of 12 000 children have been vaccinated against a disease. Calculate the percentage vaccinated.

Answers

1. Any two: neutrophils have a lobed nucleus, macrophages a large rounded one; neutrophils are short-lived, macrophages long-lived; neutrophils arrive first in large numbers; macrophages present antigens to lymphocytes.
2. Lysosomes; they release hydrolytic enzymes.
3. A molecule not found on the body’s own cells, for example on a pathogen, which the immune system recognises as foreign and responds to.
4. Each lymphocyte has receptors of one shape; only those with receptors complementary to the pathogen’s antigen are selected (clonal selection).
5. Released by T-helper cells, they stimulate matching B-lymphocytes and T-killer cells to divide (and B-cells to become plasma cells).
6. Antibodies are proteins; rough ER has ribosomes for synthesising large amounts of protein for secretion.
7. Memory cells from the first infection recognise the antigen and give a faster, larger secondary response; antibody is made quickly and the pathogen is destroyed before it causes symptoms.
8. Its amino acid sequence gives an antigen-binding site with a shape complementary to one specific antigen.
9. Plasma cells make the specific antibody but cannot divide; myeloma cells divide indefinitely, so the hybridoma both makes the antibody and can be grown in culture.
10. Artificial passive immunity. No memory cells are made, and the antibodies are broken down over a few weeks.
11. Any one: HIV mutates rapidly, so its antigens change; it lives inside T-helper cells, hidden from antibodies; it destroys the T-helper cells needed for the immune response.
12. 11 280 ÷ 12 000 × 100 = 94.0% (94%).

Where marks are usually lost

• Describing phagocytes with the wrong organelle (e.g. “ribosomes release enzymes”) instead of lysosomes.
• Missing chemotaxis or receptor binding from a description of phagocytosis.
• Saying T-helper cells or T-killer cells “produce antibodies”; only plasma cells do.
• Leaving out mitosis, clonal selection or cytokines from the primary response sequence.
• Writing that antibodies stay in the blood for years to give long-term immunity; it is memory cells that persist.
• Listing antibody parts without linking each to a function.
• Omitting the reason for fusing with myeloma cells: they divide indefinitely.
• Saying a vaccine contains antibodies or “a small dose of the disease” instead of antigens.
• Confusing natural passive (across the placenta) with artificial passive (antibody injection).
• Explaining herd immunity as “everyone is vaccinated”; it works because enough people are immune that transmission breaks down.

Official syllabus

Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027, Version 1 (published September 2022), Cambridge University Press & Assessment. Topic 11 Immunity, sections 11.1 and 11.2.