Cambridge International AS & A Level Biology 9700: Immunity – Study Guide

This study guide teaches topic 11 Immunity of the Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027. It covers section 11.1 The immune system (learning outcomes 1–4) and section 11.2 Antibodies and vaccination (learning outcomes 1–6). This is AS Level content, examined on Paper 1 (Multiple Choice) and Paper 2 (AS Level Structured Questions); the syllabus says Paper 4 also needs knowledge of AS Level content. There is no Core/Supplement split: every outcome applies to all candidates.

Useful links: Cambridge AS & A Level Biology hub, printable 9700 checklist, immunity revision notes, immunity practice questions and the free 9700 AS diagnostic. This topic builds on topic 10 Infectious diseases and on cell surface antigens from topic 4 (try the cell membranes practice questions).

What this topic covers

Syllabus section	What you must be able to do
11.1.1	Describe the mode of action of phagocytes (macrophages and neutrophils)
11.1.2	Explain what an antigen is; state the difference between self and non-self antigens
11.1.3	Describe the primary immune response, with the roles of macrophages, B-lymphocytes (including plasma cells) and T-lymphocytes (T-helper and T-killer cells only)
11.1.4	Explain the role of memory cells in the secondary response and in long-term immunity
11.2.1	Relate the molecular structure of antibodies to their functions
11.2.2	Outline the hybridoma method for producing monoclonal antibodies
11.2.3	Outline the principles of using monoclonal antibodies in diagnosis and treatment
11.2.4	Describe the differences between active and passive, and natural and artificial, immunity
11.2.5	Explain that vaccines contain antigens that stimulate immune responses to give long-term immunity
11.2.6	Explain how vaccination programmes help control the spread of infectious diseases

11.1 The immune system

Phagocytes

Phagocytes are white blood cells made in the bone marrow that engulf and digest pathogens. Their response is non-specific: any pathogen can be engulfed.

	Neutrophils	Macrophages
Nucleus	Lobed	Large, rounded or kidney-shaped
Where found	In large numbers in the blood; leave it at sites of infection	Circulate as monocytes, then settle in tissues (e.g. lungs, liver, lymph nodes) as macrophages
Lifespan	Short; die after digesting pathogens	Long-lived
Special role	Arrive first, in large numbers	Also present antigens to lymphocytes, linking non-specific and specific responses

Mode of action, step by step:

1. Damaged cells and pathogens release chemicals; the phagocyte moves towards them (chemotaxis).
2. Receptors on the phagocyte’s cell surface membrane bind to molecules on the pathogen. Binding is easier if antibodies are already attached.
3. The membrane extends around the pathogen and engulfs it by endocytosis, forming a phagocytic vacuole.
4. Lysosomes fuse with the vacuole and release hydrolytic enzymes, which digest the pathogen.
5. A macrophage keeps some antigen from the pathogen and displays it on its cell surface membrane.

Antigens: self and non-self

An antigen is a molecule, usually a protein or glycoprotein (sometimes a polysaccharide), that is recognised by the immune system and stimulates an immune response. Antigens are found on cell surface membranes (see the cell surface antigens in topic 4.1.3), on the surfaces of pathogens, and as free molecules such as toxins.

• Self antigens are found on your own cells. Your lymphocytes do not normally respond to them.
• Non-self antigens are foreign: on pathogens, on transplanted tissue from another person, or on cells in transfused blood of a different type. They stimulate an immune response.

The primary immune response

Lymphocytes give the specific response. Each lymphocyte has receptors of one shape, complementary to one antigen. There are millions of different lymphocytes, so almost any antigen matches a few of them.

Sequence of events after a pathogen enters for the first time:

1. A macrophage engulfs the pathogen and displays its antigens on its surface (it is now an antigen-presenting cell).
2. A T-helper cell with a receptor complementary to that antigen binds to it. This is clonal selection: only lymphocytes with matching receptors respond.
3. The selected T-helper cell divides by mitosis to form a clone (clonal expansion) and releases cytokines.
4. Cytokines stimulate the matching B-lymphocytes (which have also bound the antigen) to divide by mitosis.
5. Most of the B-cell clone differentiates into plasma cells. Plasma cells have a lot of rough endoplasmic reticulum and Golgi apparatus, and secrete antibodies specific to the antigen.
6. Cytokines also stimulate matching T-killer cells to divide. T-killer cells bind to body cells displaying the non-self antigen (for example, cells infected by a virus) and release substances that kill them.
7. Some B- and T-cells in each clone become memory cells.

The primary response is slow. It takes several days for enough plasma cells to form, so antibody concentration rises late and the person often has symptoms.

Memory cells and the secondary response

Memory cells are long-lived and remain in the blood and lymph. There are far more of them than there were matching lymphocytes before the first infection.

If the same antigen enters again, memory cells recognise it at once. Memory B-cells quickly divide and form plasma cells; memory T-cells quickly form T-helper and T-killer cells. This secondary response is faster, produces more antibody and lasts longer. The pathogen is usually destroyed before it causes symptoms. This is long-term immunity.

Worked example: comparing the two responses

A person is exposed to an antigen on day 0 and again on day 60. The table summarises their antibody concentrations (arbitrary units, AU).

	First exposure (day 0)	Second exposure (day 60)
Antibody first rises	Day 6 (from 0 AU)	Day 61 (from 2 AU)
Peak concentration	15 AU on day 14	240 AU on day 66

(a) How many times higher is the secondary peak?

240 ÷ 15 = 16 times higher

(b) Calculate the mean rate of increase in each response.

primary:   (15 − 0) ÷ (14 − 6)  = 15 ÷ 8   = 1.9 AU per day
secondary: (240 − 2) ÷ (66 − 61) = 238 ÷ 5 = 47.6 AU per day

(c) Explain the differences. After the first exposure, memory B-cells remained. There are many more of them than the original matching B-lymphocytes, and they are already selected, so no time is lost finding and cloning matching cells. So plasma cells form sooner and in greater numbers, and antibody rises faster (6 days to peak instead of 14) to a higher level.

11.2 Antibodies and vaccination

Antibody structure and function

Antibodies are globular glycoproteins (immunoglobulins) with quaternary structure.

Structural feature	Function it allows
Four polypeptide chains: two heavy and two light, held by disulfide bonds	A stable Y-shaped molecule
Variable region at the tip of each arm, with a different amino acid sequence in each type of antibody	Forms the antigen-binding site, complementary in shape to one specific antigen
Two antigen-binding sites	Can bind two pathogens at once, clumping them together (agglutination)
Hinge region	Flexibility, so the arms can bind antigens different distances apart
Constant region, the same in all antibodies of one class	Binds to receptors on phagocytes, marking the pathogen for engulfing

Antibodies also neutralise toxins, and can block the sites a virus uses to enter a cell.

Monoclonal antibodies: the hybridoma method

A monoclonal antibody is one type of antibody, made by a clone of identical cells. Plasma cells cannot divide, so they cannot be grown in culture. The hybridoma method solves this:

1. Inject a mouse with the chosen antigen. It makes B-lymphocytes that produce the matching antibody.
2. Remove B-lymphocytes (plasma cells) from the mouse’s spleen.
3. Fuse them with myeloma cells (cancer cells, which divide indefinitely) to form hybridoma cells.
4. Grow the cells individually and select those making the required antibody.
5. Culture the chosen hybridoma clone on a large scale and collect the identical antibody it secretes.

A hybridoma combines two abilities: to make one specific antibody (from the B-cell) and to keep dividing (from the myeloma cell).

Using monoclonal antibodies

The principle is always the same: the antibody binds only to one specific antigen.

• Diagnosis. The antibody is attached to a marker, such as a fluorescent dye, a radioactive label or a coloured particle. It binds only where its antigen is present, showing, for example, the position of a cancer or a blood clot, or detecting a pathogen or hormone in a sample. Pregnancy test strips work this way: antibodies bind the hormone hCG in urine.
• Treatment. The antibody is given to bind a specific antigen on target cells. It can block a receptor, mark cells for destruction by the immune system, or carry an attached drug or toxin straight to those cells, reducing harm to other cells. Mouse antibodies are non-self to humans, so therapeutic antibodies are altered to be more human (“humanised”) to reduce an immune response against them.

Types of immunity

	Natural	Artificial
Active (your own B-cells make antibodies; memory cells form; long-term)	Recovering from an infection such as chickenpox	A vaccine, such as a tetanus or influenza vaccine
Passive (antibodies come from outside; no memory cells; short-term)	Antibodies crossing the placenta from mother to fetus	An injection of ready-made antibodies, e.g. against rabies after a bite from an infected animal

Active immunity takes time to develop but lasts. Passive immunity is immediate but fades within weeks, because the antibodies are broken down and no memory cells are made.

Vaccines

A vaccine contains antigens that stimulate an immune response. The antigens may be in:

• live pathogens of a weakened (attenuated) strain;
• killed or inactivated pathogens;
• toxoids, harmless forms of a toxin;
• isolated antigen molecules.

The vaccine causes a primary immune response without the disease. Memory cells form, so when the real pathogen arrives, the secondary response destroys it before symptoms appear: artificial active immunity. A booster dose gives a further response and increases the number of memory cells.

Vaccination programmes

• If enough people in a population are immune, a pathogen cannot find enough susceptible hosts, so chains of transmission break. This herd immunity also protects people who cannot be vaccinated, such as newborn babies.
• Ring vaccination vaccinates everyone around each new case. It helped to eradicate smallpox.
• Problems that reduce success:
  • pathogens that change their antigens (antigenic variation, as in influenza) or have many strains, so memory cells no longer match;
  • pathogens that live inside cells, such as Plasmodium and HIV, hidden from antibodies;
  • people with a weak immune system (malnourished or with HIV) may respond poorly;
  • some vaccines must be kept cold, which is hard in remote areas;
  • not enough people take up the vaccine, so herd immunity is lost.

Common errors

• Saying phagocytes are specific, or that lymphocytes engulf pathogens.
• Writing that plasma cells or memory cells “remember” the antigen: memory cells recognise it.
• Mixing up the cells: B-cells become plasma cells, which secrete antibodies; T-killer cells kill infected cells; T-helper cells release cytokines.
• Forgetting clonal selection (only matching lymphocytes respond) and mitosis (clonal expansion).
• Calling antibodies that cross the placenta “artificial”, or saying passive immunity makes memory cells.
• Saying a vaccine contains antibodies. It contains antigens.
• Describing monoclonal antibodies without the key idea that they bind only to one specific antigen.

Where to go next

Condense this topic with the immunity revision notes, then test yourself with the immunity practice questions. Link it back to HIV and TB in the infectious diseases revision notes. Check coverage on the 9700 checklist and try the 9700 AS diagnostic.

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.