The immune system protects the body from harmful invaders (pathogens) and abnormal cells. It does this in two stages: a non-specific response (the same response to any pathogen, e.g. phagocytosis) and a specific response (involving lymphocytes, which target one particular pathogen).
Antigens
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
Each type of cell has specific molecules on its surface that identify it. These molecules include proteins and enable the immune system to identify:
- pathogens
- cells from other organisms of the same species
- abnormal body cells
- toxins.
Definition of antigen.
How does the body recognise a pathogen?
Every cell has specific molecules on its surface that act as identifiers called antigens. They can be proteins, glycoproteins, or glycolipids.
Antigens are how the immune system distinguishes self (own body cells) from non-self (foreign cells).
- Self antigens: on the body’s own cells; do not trigger an immune response
- Non-self antigens: on pathogens, transplanted cells, or abnormal body cells; do trigger an immune response
Antigens are used to detect:
- Pathogens: disease-causing organisms (bacteria, viruses, fungi)
- Cells from other organisms of the same species: important for organ transplant rejection
- Abnormal body cells: e.g. cancer cells, virus-infected cells
- Toxins: poisons (e.g. produced by some bacteria)
Definition
An antigen is a molecule (usually a protein) on the surface of a cell that triggers an immune response.
Antigen Variability
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The effect of antigen variability on disease and disease prevention.
Some pathogens (e.g. influenza, HIV) have antigens that change frequently due to mutations in the genes that code for them. This is called antigen variability.
Effects on disease and prevention:
- Memory cells from a previous infection no longer recognise the new antigen. The immune system has to respond from scratch each time, so you can catch the same disease repeatedly (e.g. flu)
- Vaccines become ineffective: last year’s flu vaccine doesn’t protect against this year’s strain, as the antigens have changed.
- This is why we often need a new flu vaccine every year
Phagocytosis (Non-specific Response)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
Phagocytosis of pathogens. The subsequent destruction of ingested pathogens by lysozymes.
Phagocytosis is the first line of defence against pathogens. It is non-specific. The same response happens to any pathogen. It’s carried out by phagocytes (a type of white blood cell).
- The phagocyte recognises non-self antigens on the pathogen and is attracted by chemicals released by the pathogen (chemotaxis)
- The phagocyte engulfs the pathogen by surrounding it with its cell-surface membrane, forming a vesicle called a phagosome
- A lysosome fuses with the phagosome
- Lysozymes (the hydrolytic enzymes inside the lysosome) hydrolyse / digest the pathogen
- The harmless products are absorbed by the phagocyte. Some antigens are displayed on the phagocyte’s surface, so it becomes an antigen-presenting cell (APC). This APC can trigger a specific immune response
Don't confuse lysosomes with lysozymes
- Lysosome = the organelle (a membrane-bound vesicle containing enzymes)
- Lysozyme = the digestive enzyme inside the lysosome that breaks down the pathogen
Specific Immune Response
After phagocytosis (non-specific response) the body launches a specific response targeted at the particular pathogen. This includes:
- Cellular response: by T lymphocytes (T cells)
- Humoral response: by B lymphocytes (B cells) and antibodies
Both are triggered by antigen-presenting cells (APCs). This is where the pathogen’s antigens are displayed on the APC’s surface.
Cellular Response (T Lymphocytes)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The response of T lymphocytes to a foreign antigen (the cellular response).
- The role of antigen-presenting cells in the cellular response.
- The role of helper T cells (T_H cells) in stimulating cytotoxic T cells (T_C cells), B cells and phagocytes. The role of other T cells is not required.
T lymphocytes mature in the thymus. A T cell with a complementary receptor binds to the antigen displayed on an Antigen Presenting Cell (APC), which activates the T cell.
Cellular Response Process
- An antigen-presenting cell (e.g. a phagocyte, as we just looked at) displays the pathogen’s antigen on its surface. Note: This could be other antigen-presenting cells (e.g. cells infected by virus, cancer cells, foreign cells).
- A helper T cell with a complementary receptor binds to the antigen (clonal selection)
- This activates the helper T cell, which divides by mitosis (clonal expansion). This produces many identical helper T cells.
- The activated helper T cells then stimulate:
- Cytotoxic T cells: these kill virus-infected cells and tumour cells (see below)
- B cells: to start the humoral response (see below)
- Phagocytes: to perform more phagocytosis
- Note: For the AQA spec you don’t need to know the role of other T cells (e.g. regulatory T cells)
- Some of the cloned T cells become memory T cells, ready for a rapid response to any future infection by the same pathogen
Cytotoxic T Cell
- These destroy abnormal (e.g. cancer cells) or infected cells
- They do this by releasing a protein called perforin
- This forms a pore in the cell-surface membrane, which allows substances to freely enter and leave the cell, and as a result the cell dies
Humoral Response (B Lymphocytes)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The response of B lymphocytes to a foreign antigen, clonal selection and the release of monoclonal antibodies (the humoral response).
B lymphocytes mature in the bone marrow. Each B cell has a unique antibody on its surface (a B cell receptor) that’s complementary to one specific antigen.
One B cell: one antibody specificity
Every B cell carries many identical antibodies on its surface. They all bind the same antigen. Different B cells carry different antibodies, so collectively the body has millions of B cells, each able to recognise a different antigen.
Humoral Response Process
- A B cell with the complementary receptor (this is the antibody on its surface) binds to the foreign antigen
- This is clonal selection. The antigen “selects” the B cell with the matching antibody
- The B cell takes in the antigen (internalises it), processes it, and presents it on its surface
- This is now an antigen-presenting cell (APC)
- A helper T cell binds to this same B cell (APC) and activates it
- (Extra detail: T helper cells release cytokines which activate the B cell)
- The activated B cell divides by mitosis
- This is clonal expansion, which produces many identical clones of the selected B cell
- The clone of B cells differentiates into:
- Plasma cells: secrete large numbers of monoclonal antibodies (all identical, specific to the original antigen)
- Memory cells: stay in the blood long-term, ready for a rapid response to any future infection by the same pathogen
What is the difference between clonal selection and clonal expansion?
What is the difference between clonal selection and clonal expansion?
Easy to mix these up:
- Clonal selection = the antigen selects the B (or T) cell with the matching receptor. This happens at binding (step 1).
- Clonal expansion = the selected cell then divides by mitosis to produce many identical clones. This happens at step 4.
Think: select first, then expand. You can’t multiply a cell until you’ve picked the right one.
Antibodies
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
- Definition of antibody.
- Antibody structure.
- The formation of an antigen-antibody complex, leading to the destruction of the antigen, limited to agglutination and phagocytosis of bacterial cells.
All the monoclonal antibodies produced by the plasma cells are identical and bind to the same specific antigen on the pathogen, so they can be used by the immune system to destroy that specific pathogen.
Definition
An antibody is a protein (specifically, a quaternary-structure protein) produced by plasma cells that binds to a specific antigen.
Monoclonal means identical antibodies. These are produced from a single clone of plasma cells, so they all bind to the same specific antigen.
Antibody Structure
- Antibody is a quaternary protein, made of 4 polypeptide chains: 2 heavy and 2 light chains
- These chains are held together by disulfide bridges
- There are two identical variable regions, with the antigen-binding sites at the tips
- The variable region’s amino acid sequence is specific to one type of antigen, so one antibody can only bind to one type of antigen
- The rest of the molecule is the constant region (the same in all antibodies)
Why are antibodies important?
When an antibody binds to its specific antigen, they form an antigen-antibody complex. The pathogen is then destroyed in two ways:
- Agglutination: each antibody has two binding sites, so it can stick to two bacteria at the same time, acting as a bridge between them. Many antibodies doing this clump the bacteria together, making them too big to enter cells and easier for phagocytes to engulf
- Phagocytosis: the clumped pathogens are then engulfed and destroyed by phagocytes (as above)
Antibodies can also neutralise toxins released by bacteria, binding to the toxin and preventing it from affecting cells.
Primary vs Secondary Immune Response
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The roles of plasma cells and of memory cells in producing primary and secondary immune responses.
Your body reacts differently depending on whether it’s the first time a specific pathogen enters the body, or whether you have already encountered it before.
Primary Response (Slow, Fewer Antibodies)
- The first time the body meets a pathogen is called the primary response.
- It is generally slow, and creates only a few antibodies.
- Why? Because it has to go through the humoral response process, where the correct B cell needs to be selected (clonal selection) and then divide by mitosis (clonal expansion) to produce plasma cells, which can then produce antibodies. After this has happened, memory cells are produced.
- The person often shows symptoms of the disease.
Secondary Response (Faster, Lots of Antibodies)
- The next time the body meets the same pathogen is called the secondary response.
- It’s faster and creates lots of antibodies, often clearing the infection before symptoms appear.
- Because memory cells are already specific to the antigen and there are many of them, clonal selection is much faster. The memory cells are able to recognise the antigen almost immediately, then divide rapidly into plasma cells.
| Primary response | Secondary response | |
|---|---|---|
| Speed | Slower | Faster |
| Antibody concentration | Low | Much higher |
| Symptoms | Often experienced | Usually none |
| Why | First exposure: no memory cells yet | Memory cells divide rapidly into plasma cells |
Vaccination
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The use of vaccines to provide protection for individuals and populations against disease. The concept of herd immunity.
A vaccine contains antigens from a pathogen in a form that can’t cause disease, usually a dead (inactivated) or weakened pathogen. The body responds as if it’s a real infection, producing a primary immune response, which produces memory cells.
If the person later meets the real pathogen, they have a secondary immune response straight away, so they don’t develop symptoms.
Herd Immunity
If a large enough proportion of the population is vaccinated, the pathogen can’t spread easily. Even people who aren’t vaccinated are protected because they’re unlikely to come into contact with the pathogen.
This is important for:
- People who can’t be vaccinated (e.g. infants, the immunocompromised)
- Stopping outbreaks spreading through a population
Active vs Passive Immunity
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The differences between active and passive immunity.
| Active immunity | Passive immunity | |
|---|---|---|
| How antibodies are made | The person’s own immune system produces them | Antibodies given from another source |
| Memory cells made? | Yes, so long-term protection | No, so only short-term protection |
| Speed of protection | Slow (takes time to produce antibodies) | Fast (antibodies are already present) |
Quick way to remember
- Active = active immune system (you do the work), so you create memory cells and have long-term protection
- Passive = passive recipient (you’re given the antibodies), so have no memory cells, and only short-term protection
Can you name some examples of active vs passive immunity?
Can you name some examples of active vs passive immunity?
- Active immunity:
- Catching a disease naturally (e.g. chickenpox)
- Vaccination
- Passive immunity:
- Antibodies passed from mother to baby (across the placenta and in breast milk)
- Anti-venom / anti-toxin injections (e.g. for snake bites, tetanus)
How this topic is tested
This analysis is based on past paper data from 2017 to 2025. It is intended for interest only and is not predictive of what will appear in future papers.
- Tested in 9 of 9 years (2017–2025): 47 question parts worth 113 marks.
- 1st most-examined topic overall by marks, 1st in Unit 2.
Marks by year
Most-tested spec points
- Humoral Response: B Lymphocytes: tested in 10 parts (28 marks)
- Antibody Structure & Action: tested in 8 parts (19 marks)
- Cellular Response: T Lymphocytes: tested in 6 parts (17 marks)
- HIV Structure & Replication: tested in 5 parts (15 marks)
- Cell Recognition & Antigens: tested in 6 parts (13 marks)
- Uses of Monoclonal Antibodies: tested in 5 parts (13 marks)
Also links to: Structure of Viruses, Evaluating the Use of Stem Cells, Evaluating Cancer Evidence & Treatment.
Maths and practical skills
- Units and standard form (MS 0.1, 0.2): e.g. calculate the volume of antibody solution to inject into a 23 g mouse, in dm³ and in standard form 2021 P1 Q7.3
- Percentages, ratios and fractions (MS 0.3): e.g. use a calculation to decide whether horses or rabbits are better for producing antivenom 2018 P1 Q7.3
- Standard deviation and range (MS 1.10): e.g. plot a graph of mean increase in ear thickness, including ± 2 standard deviations 2023 P3 Q6.3
- Tables, bar charts and histograms (MS 1.3): e.g. plot a suitable graph for mean increase in ear thickness in each group of mice 2023 P3 Q6.3
- Averages (MS 1.6): e.g. use median values to calculate a difference in the number of B cells per dm³ 2018 P3 Q2.3
- Choosing and using a statistical test (MS 1.9): e.g. choose a statistical test to find out if there is a significant relationship between CD20 on B cells and the percentage of B cells destroyed, and give a reason 2018 P3 Q2.1
Tips from examiner reports
What students commonly get wrong
Antigens
- Cells that stimulate an immune responseWatch out: when asked which types of cell can stimulate an immune response, don't name B cells and T cells: those are the cells that respond. The cells that stimulate a response are ones with antigens the body recognises as foreign: pathogens, cells from other people or other species, abnormal body cells and antigen-presenting cells. 2023 P3 Q6.1
Antibodies
- Antibodies have a binding site, not an active siteWatch out: antibodies have a binding site, not an active site. Don't describe an antigen-antibody complex as an "enzyme-substrate" or "antibody-substrate" complex. 2020 P1 Q7.3 · 2022 P1 Q3.6
B cells and the humoral response
- Plasma cells make antibodiesWatch out: antibodies are made by plasma cells, which develop from B cells, not T cells. B cells don't become macrophages. 2018 P1 Q7.5 · 2020 P3 Q3.4
Active and passive immunity
- Antivenom is passive immunityWatch out: antivenom gives passive immunity: the antibodies are given ready-made. It isn't a vaccine, so it doesn't trigger the person's own immune response, and active immunity would be too slow to help after a bite. 2018 P1 Q7.1
Exam Question Practice
A few exam-style questions on this topic to try. Have a go at each one before opening the answer.
A group of closely related viruses used to infect only one species of bat.
These viruses are now found infecting several other species of bat.
Suggest and explain how the viruses became able to infect other species of bat.
(2 marks)
Hint
What part of a virus has to fit the host cell for infection to happen? What could change that part?
Mark Scheme
Max 2 marks
- Mutation in the viral DNA/RNA/genome/genetic material (1 mark)
- Altered (tertiary structure of the) viral attachment protein (1 mark)
- Allows it/the attachment protein/the virus to bind (to receptors of other species) (1 mark)
Also accepted / rejected
Tips
- ‘The virus mutates’ isn’t enough: say the mutation is in the viral DNA or RNA and changes the attachment protein
- Link the change to infection: the new attachment protein can bind to receptors on cells of other bat species
- This is about infecting new species, not about how viruses replicate or evade a secondary immune response
Describe how phagocytosis of a bacterium leads to presentation of its antigens.
(3 marks)
Hint
After the bacterium is engulfed, what fuses with the phagosome, and what happens to the bacterium? Where do its antigens end up?
Mark Scheme
- Phagosome/vesicle fuses with a lysosome (1 mark)
- (Bacterium) destroyed by lysozymes/hydrolytic enzymes (1 mark)
- Peptides/antigens (from the bacterium) are displayed on the cell membrane (1 mark)
Also accepted / rejected
1. Accept vacuole fuses with lysosome. Reject “the bacterium fuses with a lysosome”.
Tips
- Keep to the question asked, rather than the whole immune response
- Finish by saying the antigens are displayed on the phagocyte’s cell-surface membrane
Describe how presentation of a bacterial antigen leads to the secretion of an antibody against this bacterial antigen.
(3 marks)
Hint
Which cell binds to the presented antigen first? Which cell does it then stimulate, and what does that cell become?
Mark Scheme
Max 3 marks
- Helper T cell/TH cell binds to the antigen (on the antigen-presenting cell/phagocyte) (1 mark)
- This helper T/TH cell stimulates a specific B cell (1 mark)
- The B cell clones
OR The B cell divides by mitosis (1 mark) - (Forming) plasma cells that release antibodies (1 mark)
Also accepted / rejected
1 and 2. “Helper” is only needed once.
2. Accept “this (helper) T cell stimulates a competent B cell” OR “T cell stimulates B cell to undergo clonal selection”. This statement gains both mark points 2 and 3.
Tips
- Don’t describe presentation again: start with the helper T cell binding to the presented antigen
- Include the T cell’s role: it stimulates a specific B cell, which then divides by mitosis into plasma cells that secrete antibodies
Botulinum toxin is made by some bacteria and can cause paralysis. Patients with botulism are treated with an injection of antitoxin. Antitoxin contains antibodies against botulinum toxin. This treatment is an example of passive immunity.
Explain how treatment with antitoxin works and why it is essential to use passive immunity, rather than active immunity.
(2 marks)
Hint
What do the injected antibodies do to the toxin? Why couldn’t the patient wait for their own immune response?
Mark Scheme
- (Antitoxin/passive immunity) antibodies bind to the toxin/antigen and (cause) its destruction (1 mark)
- Active immunity would be too slow/slower (1 mark)
Also accepted / rejected
1. For bind accept attach; ignore attack.
1. For destruction of the toxin accept agglutination or phagocytosis.
1. Ignore reference to antibodies “neutralising the toxin/stopping damage”. Reject reference to “killing” the toxin.
2. Accept “passive immunity is faster”, but not simply “passive immunity is fast”.
Tips
- Give both parts of the first mark: the antibodies bind to the toxin and this leads to its destruction; ‘complementary’ isn’t the same as binding
- Make it comparative: active immunity would be too slow, not just ‘takes time’
- Antitoxin isn’t a vaccine and doesn’t trigger an immune response
Antitoxin is produced by vaccinating horses with a harmless form of botulinum toxin, so they produce antibodies against it. These antibodies are then extracted and used to treat patients.
During vaccination, each horse is first injected with a small dose of the harmless toxin. Three weeks later, it is injected with a larger dose.
Use your knowledge of the humoral immune response to explain this vaccination programme.
(3 marks)
Hint
Which cells respond to the toxin antigen, and what do they divide into? How is the response to the second dose different?
Mark Scheme
- B cells specific to the toxin divide by mitosis (1 mark)
- (B cells produce) plasma cells and memory cells (1 mark)
- The second dose produces antibodies (in a secondary immune response) in a higher concentration and more quickly
OR The first dose must be small so the horse is not killed (1 mark)
Also accepted / rejected
1. Accept in the context of the primary or secondary immune response.
1. Credit the idea of specificity if given once in relation to T or B cells. Accept a description of specificity.
1. Accept clone for divide by mitosis. “Clonal selection of B cells” = mark point 1.
3. Accept “a lot of antibody” for a higher concentration of antibody.
Tips
- Include specificity: B cells specific to the toxin antigen divide by mitosis (clone)
- B cells, not T cells, become plasma cells that produce antibodies, and memory cells
- For the second dose, say antibodies are produced both more quickly and in a higher concentration
1. Accept named examples of mutations.
2. Accept antigen for attachment protein. Accept “causes antigenic variability”.
3. Accept descriptions of binding, e.g. is complementary.