OCR A Level Biology A: Specific immunity, vaccination and medicines (H420)

This guide covers learning outcomes 4.1.1(f) to 4.1.1(n) of the OCR A Level Biology A (H420) specification, Version 4.1 (April 2026), for first assessment in 2025. They sit in the module on biodiversity, evolution and disease. The specification lists Biological diversity (Component 02) as assessing modules 1, 2, 4 and 6, and Unified biology (Component 03) as assessing all six modules. Statement 4.1.1(e), on phagocytes, comes just before this unit, and only the parts needed here are recalled. Use the revision notes and the practice questions alongside it. The course hub, the printable checklist and the free diagnostics show the rest of the course. Protein structure is revised in the Foundations in Biology guide.

What this guide covers

Outcome	What you must be able to do
4.1.1(f)	Describe the structure, roles and modes of action of B and T lymphocytes, including cell signalling, clonal selection and expansion
4.1.1(g)	Explain primary and secondary responses, including memory cells
4.1.1(h)	Describe antibody structure and general functions
4.1.1(i)	Outline the action of opsonins, agglutinins and anti-toxins
4.1.1(j)	Distinguish active, passive, natural and artificial immunity, with examples
4.1.1(k)	Explain autoimmune disease, with arthritis as an example
4.1.1(l)	Explain vaccination, vaccination programmes and why they change
4.1.1(m)	Describe sources of medicines and personalised medicine
4.1.1(n)	Evaluate the benefits and risks of antibiotics

B and T lymphocytes (4.1.1(f))

Lymphocytes are white blood cells made in the bone marrow. Each one carries receptors of a single shape on its surface. A B lymphocyte (B cell) has receptors that are antibody molecules fixed in the membrane. A T lymphocyte (T cell) has T cell receptors. Because the receptors are made before any infection, a very large range of shapes already exists in your body.

An antigen is a molecule, usually a protein on the surface of a pathogen, that triggers an immune response. An antigen-presenting cell (APC) takes in a pathogen, then displays pieces of its antigens on its own surface membrane.

The sequence of the specific response

1. A T helper cell with a receptor complementary to the displayed antigen binds to the APC. Only this cell is selected: this is clonal selection.
2. The T helper cell divides by mitosis to make a clone of identical cells: clonal expansion.
3. T helper cells release cytokines, including interleukins. This is cell signalling: a chemical message carried from one cell to another.
4. Cytokines stimulate B cells that have bound the same antigen to divide and differentiate. Cytokines also activate T killer cells and attract and stimulate phagocytes.
5. Most of the B cell clone becomes plasma cells, which secrete large quantities of one antibody. A few become B memory cells.

The cells and their roles

Cell	Role
T helper	Releases cytokines that coordinate the response
T killer	Recognises and destroys body cells that display the antigen, such as virus-infected cells
T memory	Long-lived, stays ready for the same antigen
Plasma cell	Makes and secretes antibodies. It has abundant rough endoplasmic reticulum and Golgi apparatus, because it makes so much protein for export
B memory	Long-lived, stays ready for the same antigen

T cells provide the cell-mediated response, because the cells themselves act. B cells provide the humoral response, because antibodies in body fluids act.

Primary and secondary responses (4.1.1(g))

On first exposure few lymphocytes match the antigen, so selection and expansion take days. The primary response is slow and small, and the patient may become ill. B memory and T memory cells are left behind. On re-exposure there are many more matching cells and they respond to a smaller dose. The secondary response begins sooner, rises faster, reaches a higher peak and lasts longer, usually before symptoms appear.

Worked example: comparing two responses

An animal receives an antigen on day 0 and the same antigen on day 60. Antibody concentration is in arbitrary units (AU).

Event	Result
First exposure	First detected on day 5; peak of 30 AU on day 15
Second exposure	20 AU on day 61; peak of 750 AU on day 67

Rate of rise, first response  = (30 - 0) / (15 - 5)    = 3.0 AU per day
Rate of rise, second response = (750 - 20) / (67 - 61) = 121.7, so 122 AU per day
Peak ratio = 750 / 30 = 25 times higher

Explanation: the first exposure left B memory cells. They are already selected and are present in large numbers, so no time is spent finding a matching cell. They divide and form plasma cells at once. A vertical axis that covers a huge range is often drawn as a log scale, so equal steps then mean equal multiples, not equal amounts.

Antibodies (4.1.1(h))

Antibodies are globulin proteins, also called immunoglobulins, made by plasma cells. Each has quaternary structure and four polypeptide chains:

• two identical heavy chains and two identical light chains, held together by disulfide bridges;
• a Y shape, with a flexible hinge region where the arms join the stem;
• a variable region at the tip of each arm, whose amino acid sequence gives a binding site complementary to one antigen, so one molecule has two identical binding sites;
• a constant region that is the same in antibodies of one class. Cells such as phagocytes recognise it.

The specificity comes from tertiary structure in the variable region, as with an enzyme and its substrate. A different antigen does not fit. General functions: bind to antigens, mark pathogens for destruction, and neutralise toxins.

Opsonins, agglutinins and anti-toxins (4.1.1(i))

Type	Outline of action
Opsonins	Bind to the surface of a pathogen. Phagocytes have receptors for them, so the pathogen is engulfed more readily
Agglutinins	Cause pathogens to clump together (agglutination). Each antibody has two binding sites, so it can link two cells. Clumps are engulfed easily and cannot spread as freely
Anti-toxins	Bind to toxins released by bacteria and neutralise them, so the toxin can no longer bind to its target cells

Types of immunity (4.1.1(j))

Active immunity: your own immune system makes the antibodies and memory cells. Passive immunity: you receive antibodies made by another individual. Natural immunity happens in everyday life. Artificial immunity results from a medical procedure.

	Active	Passive
Natural	Recovering from chickenpox	Antibodies across the placenta; antibodies in breast milk
Artificial	A vaccine	Injection of antibodies such as tetanus immunoglobulin or antivenom

Active immunity is slow to start and long-lasting, because memory cells form. Passive immunity acts immediately but is short-lived. The recipient made no memory cells, and the antibodies are broken down.

Autoimmune disease (4.1.1(k))

An autoimmune disease happens when the immune system fails to distinguish self from non-self and attacks the body’s own tissues. In rheumatoid arthritis, the immune system attacks tissues in the joints, causing inflammation, pain and damage to cartilage. Treatment often uses drugs that suppress immune activity. The cost is a greater risk of infection.

Vaccination (4.1.1(l))

A vaccine contains antigens from a pathogen (for example weakened or killed pathogens, a toxin made harmless, or a purified surface protein). It gives artificial active immunity. The primary response forms memory cells without disease, so a later infection triggers a secondary response. A booster dose reinforces the memory.

Herd immunity occurs when enough people are immune that a pathogen cannot spread easily, which also protects people who cannot be vaccinated. A simple model gives the proportion that must be immune as 1 - 1/R₀, where R₀ is the number of people one case infects in a fully susceptible population.

Worked example: vaccine trial

In a trial, 25 000 people receive a vaccine and 25 000 receive a placebo. Over a season, 40 vaccinated and 320 placebo participants get the disease.

Rate, vaccinated = 40 / 25 000  = 0.16 %
Rate, placebo    = 320 / 25 000 = 1.28 %
Reduction = (1.28 - 0.16) / 1.28 x 100 = 87.5 %

Worked example: herd immunity

A disease has R₀ = 6. A vaccine protects 95 % of those who receive it.

Proportion immune needed = 1 - 1/6 = 0.833 (83.3 %)
Coverage needed = 83.3 / 0.95 = 87.7 %, about 88 % of the population

Programmes and why they change

Routine vaccinations protect against diseases such as measles, mumps, rubella, diphtheria, tetanus, whooping cough and polio. Epidemics are prevented by keeping coverage high. Programmes change because:

• pathogens change, so influenza vaccines are updated as surface antigens vary, and new diseases need new vaccines;
• a disease can be eradicated, as smallpox was, so vaccination can stop;
• coverage can fall, for example through misinformation, and outbreaks follow;
• global issues: cost, storage and transport needs, conflict, and travel spreading disease across borders.

Sources of medicines (4.1.1(m))

Many medicines come from living organisms. Plants provide examples: willow bark gave salicin, from which aspirin was developed, and foxglove provides digoxin. Microorganisms provide others: the fungus Penicillium makes penicillin, and soil bacteria of the genus Streptomyces make several antibiotics. Species not yet studied may contain useful chemicals. Extinction could remove them, which is one reason to maintain biodiversity.

Personalised medicine uses a person’s genome to choose a drug or dose. People differ in the alleles that affect how a drug is absorbed, broken down or targeted, so treatment can be more effective with fewer side effects. Limits are cost, access to sequencing and protecting genetic data.

Antibiotics (4.1.1(n))

Antibiotics treat bacterial infection and do not work on viruses. After penicillin was discovered in the mid-20th century, antibiotics were widely used. Deaths from bacterial infections fell, and surgery and cancer treatment became safer.

Benefits: treat infection, save lives, allow major surgery. Risks: allergic reactions, side effects, killing harmless gut bacteria, and resistance.

How resistance spreads

A mutation by chance gives a bacterium resistance. The antibiotic kills the sensitive bacteria and the resistant one survives and reproduces. Resistance alleles pass to offspring and, on plasmids, to other bacteria. The implications are infections that are harder to treat, such as MRSA, longer illness and higher cost.

Worked example: selection

A culture contains 2.0 x 10⁹ bacteria. One in 10⁸ is resistant. The antibiotic kills all sensitive cells, and the survivors double every 30 minutes for 8 hours.

Resistant at start = 2.0 x 10^9 / 10^8 = 20
Doublings in 8 h = 16
Resistant after 8 h = 20 x 2^16 = 1 310 720, about 1.3 x 10^6

Reducing resistance: use antibiotics only when needed and as prescribed, do not use them for viruses, prevent infection by hygiene and vaccination, and develop new antibiotics.

Common errors

• Saying antibodies are “killed” or “alive”. They are proteins.
• Saying bacteria “become resistant” because of exposure. Resistant mutants already exist and are selected.
• Mixing up the cells: T killer cells destroy infected cells, plasma cells make antibodies.
• Calling a vaccine “passive” because it is injected.
• Saying memory cells are antibodies.

Official syllabus

OCR, A Level Biology A (H420) specification, Version 4.1 (April 2026), first assessment 2025: learning outcomes 4.1.1(f) to 4.1.1(n).