OxfordAQA International AS and A-level Biology: Immunity: antigens, antibodies and vaccination (9610)

This study guide is aligned to the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1 (International AS exams May/June 2017 onwards, International A-level exams May/June 2018 onwards). It covers section 3.2.5, the defensive functions of mammalian blood, in three parts: 3.2.5.1 the principles of immunology, 3.2.5.2 the response of B cells to a foreign antigen, and 3.2.5.3 vaccination. Section 3.2.5 sits in Unit 2, Biological systems and disease, which the specification places in both the International AS and the International A-level.

Use it with the revision notes and the practice questions. The course hub is OxfordAQA A-level Biology, the printable checklist tracks your progress, and the free diagnostics show where to start. For the pathogens that trigger these responses, see causes of disease.

What this unit covers

Section	What you must be able to do
3.2.5.1	Explain how cell-surface molecules identify cells; define antigen; explain the effect of antigen variability on disease and its prevention; distinguish T cells (cell-mediated immunity) from B cells (humoral immunity); describe phagocytosis and digestion by lysosomes
3.2.5.2	Describe the role of antigen-presenting cells; define antibody and describe its structure; explain how the antigen-antibody complex leads to destruction of bacterial cells by agglutination and phagocytosis
3.2.5.3	Explain the roles of plasma cells and memory cells in the primary and secondary response; explain how vaccines protect individuals and populations, including herd immunity; distinguish active from passive immunity; evaluate methodology, evidence and data from vaccine trials

3.2.5.1 The principles of immunology

Cell-surface molecules and identity

Every cell carries specific molecules on its surface, many of them proteins. These act as an identity badge. The immune system uses them to recognise:

• pathogens and toxins
• cells from other organisms of the same species (for example, transplanted tissue from a donor who is not genetically identical)
• abnormal body cells, such as cells infected by a virus or cancer cells.

Your own cells carry “self” molecules, so the response is aimed at “non-self” molecules.

Antigens

An antigen is a molecule, usually a protein, that is recognised as foreign and stimulates an immune response. Antigens sit on the surface of pathogens, are part of toxins, and are found on foreign or abnormal cells. Each antigen has a specific three-dimensional shape, which is why each lymphocyte and antibody recognises only one.

Antigen variability

Some pathogens change their antigens. This matters in two ways.

1. Disease. If a pathogen’s antigen changes by mutation, memory cells made against the old antigen no longer bind it. The person can be infected again with the “new” strain. Influenza is the standard example: its surface antigens change, so new strains keep appearing.
2. Prevention. A vaccine contains specific antigens. If the circulating pathogen has different antigens, the vaccine gives little protection. Influenza vaccines are therefore updated and given again, and a vaccine against a very variable pathogen such as HIV is hard to design.

T cells and B cells

Both are lymphocytes. The two types of response work together.

Feature	Cell-mediated immunity	Humoral immunity
Main cells	T cells	B cells
Acts on	Body cells that carry foreign antigens, for example virus-infected cells	Antigens free in blood and tissue fluid
Main product	Responses by T cells themselves	Antibodies, released into the blood

Humoral immunity is called that because it works through antibodies carried in body fluids (“humours”). B cells are primarily responsible for it. T cells are needed to start the B cell response, as section 3.2.5.2 explains.

Phagocytosis and lysosomes

Phagocytes such as neutrophils and macrophages engulf and digest pathogens.

1. Chemicals from the pathogen attract the phagocyte, and receptors on its surface bind to the pathogen.
2. The cell surface membrane folds round the pathogen and engulfs it, forming a vacuole called a phagosome.
3. Lysosomes fuse with the phagosome and release hydrolytic enzymes (including lysozyme) into it.
4. The enzymes digest the pathogen. Useful products are absorbed into the cytoplasm.

Lysosomes are membrane-bound organelles from the Golgi apparatus that hold the enzymes safely away from the rest of the cell. A macrophage then displays pathogen antigens on its own surface, which leads into the next section.

3.2.5.2 The response of B cells to a foreign antigen

Antigen-presenting cells

An antigen-presenting cell displays foreign antigens on its surface after taking in and processing a pathogen. A macrophage is a typical example, and so is a body cell infected by a virus, which displays viral antigens. T cells have receptors that bind to a particular antigen displayed this way. This step links the non-specific response (phagocytosis) to the specific response.

Sequence of the B cell response

1. A pathogen is engulfed by a macrophage, which presents its antigen.
2. A T cell whose receptor is complementary to that antigen attaches to the presenting cell and becomes activated. These T cells then help to stimulate B cells.
3. A B cell with a surface antibody complementary to the same antigen binds it. Each B cell makes one type of antibody, so only a few B cells fit a given antigen.
4. The selected B cell divides repeatedly by mitosis (clonal expansion), giving many identical cells.
5. Most of the clones become plasma cells, which secrete large amounts of one antibody. Some become memory cells (section 3.2.5.3).

Antibodies

An antibody is a protein (an immunoglobulin) made by plasma cells that binds specifically to one antigen.

Structure of a typical antibody:

• Four polypeptide chains (two identical long heavy chains, two identical shorter light chains) joined by disulfide bridges.
• The molecule is Y-shaped. The two arms each end in a variable region. Its amino acid sequence differs between antibodies, so its tertiary structure forms an antigen-binding site complementary to one antigen. There are two identical binding sites per antibody.
• A constant region, which does not vary within a class of antibodies.
• A flexible hinge region at the junction of the arms.

A different primary structure in the variable region gives a different binding-site shape, so each antibody is specific.

The antigen-antibody complex

When an antibody binds its antigen it forms an antigen-antibody complex. For bacterial cells, this leads to destruction in two linked ways.

• Agglutination. An antibody has two binding sites and can therefore attach to two bacterial cells at the same time. Many antibodies link many cells into clumps. Clumped cells cannot spread easily and are easier to engulf.
• Phagocytosis. Phagocytes bind to the antibodies coating the bacteria and engulf them, and the cells are digested by lysosomes as above.

3.2.5.3 Vaccination

Primary and secondary response

The first time you meet an antigen, the primary response is slow. Few B cells fit the antigen, so there is a lag before antibody concentration rises, and the peak is low. Some clones become memory cells, which persist for years.

On the next exposure, memory cells recognise the antigen quickly, divide rapidly and form plasma cells. The secondary response therefore starts sooner, rises faster, reaches a much higher peak and lasts longer. The pathogen is usually destroyed before symptoms appear.

Cell	Role
Plasma cell	Secretes large quantities of antibody; short-lived
Memory cell	Long-lived; gives the rapid, larger secondary response

Vaccines and herd immunity

A vaccine contains antigens from a pathogen (a weakened or killed whole organism, or purified antigens) but cannot cause the disease. It triggers the primary response and creates memory cells, so a later infection triggers a secondary response. Booster doses strengthen memory.

Herd immunity. When a high proportion of a population is immune, a pathogen cannot pass easily between susceptible people. This protects people who are not immune, such as babies too young to be vaccinated and people who cannot be vaccinated for medical reasons. Protection of a population depends on how many people are vaccinated and how well the vaccine works.

Active and passive immunity

	Active immunity	Passive immunity
Source of antibodies	Your own plasma cells	Another individual
Memory cells	Formed	Not formed
Onset	Slow	Immediate
Duration	Long term	Short term, as antibodies are broken down
Examples	Infection; vaccination	Antibodies crossing the placenta or in breast milk; injected antibodies

Evaluating vaccine trials

You may be asked to judge methodology, evidence and data. Points to look for:

• Control. A placebo group, or a group given an existing vaccine, lets you attribute differences to the vaccine.
• Randomisation and blinding. Random allocation avoids bias in who gets the vaccine; double-blind testing stops expectations affecting results.
• Sample. Large, representative groups make results more reliable and let you generalise. Check age, sex and health status.
• Outcome measured. Antibody concentration shows an immune response; fewer cases of disease shows protection. Disease incidence is the stronger evidence.
• Duration. Short follow-up cannot show how long protection lasts.
• Safety. Compare side effects between groups.
• Statistics. A difference needs a suitable statistical test before you can call it significant.

Worked examples

Example 1: vaccine efficacy

In a trial, 6,000 people received a vaccine and 9 developed the disease. In a placebo group of 6,000 people, 72 developed it. Calculate the efficacy.

Attack rate, vaccine  = 9 / 6000 x 100  = 0.15 %
Attack rate, placebo  = 72 / 6000 x 100 = 1.2 %
Efficacy = (1.2 - 0.15) / 1.2 x 100     = 87.5 %

The vaccine reduced the risk of disease by 87.5%.

Example 2: how much of a population must be immune?

A simple model gives the minimum immune fraction as 1 - 1/R, where R is the mean number of new infections caused by a single case when nobody is immune. If R = 6:

1 - 1/6 = 0.8333, so 83.3 % must be immune.

If the vaccine protects only 90 % of those given it, coverage must be 83.3 / 0.9 = 92.6 %.

Example 3: reading an antibody graph

A person’s antibody concentration peaks at 12 arbitrary units after a first exposure and at 480 units after a second.

Fold increase = 480 / 12 = 40

The secondary peak is 40 times higher. Explain: memory cells from the first exposure divide quickly and form many plasma cells.

Common errors

• Writing that antibodies “kill” bacteria. They bind, cause agglutination and mark cells for phagocytosis.
• Saying a vaccine contains antibodies. It contains antigens.
• Saying memory cells make antibodies directly. They divide and become plasma cells on re-exposure.
• Describing herd immunity as everybody being immune.
• Calling a placebo group “unvaccinated and untreated”. It receives an inactive injection so participants cannot tell which group they are in.

Official syllabus

OxfordAQA, International AS and A-level Biology (9610), Version 5.1: sections 3.2.5.1, 3.2.5.2 and 3.2.5.3. This page is an independent Marlbridge resource and is not endorsed by OxfordAQA.