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

These notes condense 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. For full explanations, use the study guide. Test yourself with the practice questions. The course hub, the printable checklist and the free diagnostics help you plan. Antibody structure builds on protein structure in the Foundations in Biology revision notes.

Key terms

Term	Meaning
Antigen	A foreign molecule, often a surface protein of a pathogen, that starts an immune response
Antigen-presenting cell	A cell that displays antigen fragments on its surface membrane
Clonal selection	Only lymphocytes with a complementary receptor are activated
Clonal expansion	The selected lymphocyte divides by mitosis to form a clone
Cytokine	A signalling protein released by a cell to change the behaviour of another cell. Interleukins are cytokines
Plasma cell	A differentiated B cell that secretes antibody
Memory cell	A long-lived B or T cell that gives a fast secondary response
Epidemic	A rapid rise in cases of a disease in a population

4.1.1(f) Lymphocytes: the sequence

1. An antigen-presenting cell displays an antigen.
2. A T helper cell with a complementary receptor binds. Clonal selection, then clonal expansion.
3. T helper cells release cytokines (interleukins): cell signalling.
4. Cytokines activate B cells that bound the same antigen, activate T killer cells and stimulate phagocytes.
5. B cells form plasma cells (antibodies) and B memory cells.
6. T killer cells destroy infected body cells. T memory cells remain.

Humoral response: antibodies in body fluids, from B cells. Cell-mediated response: whole T cells acting on target cells.

Plasma cell adaptation: abundant rough endoplasmic reticulum and Golgi apparatus, to make and secrete protein.

4.1.1(g) Primary and secondary responses

Feature	Primary	Secondary
Starts	Several days after exposure	Much sooner
Rate of rise	Slow	Fast
Peak antibody	Low	Much higher
Duration	Shorter	Longer
Symptoms	Often present	Often absent
Reason	Few matching cells	Many B and T memory cells

Method: reading an antibody graph

1. State the time to first detection for each response.
2. Read both peak values and say “x times higher” (divide).
3. Rate = change in concentration / change in time, from two points on the steepest part.
4. Link the differences to memory cells.

Worked reminder

First dose: 0 to 12 AU between day 4 and day 14. Second dose: 5 to 640 AU between day 1 and day 6 after it.

Rate 1 = 12 / 10 = 1.2 AU per day
Rate 2 = (640 - 5) / 5 = 127 AU per day
Rate 2 / Rate 1 = 127 / 1.2 = 106 times faster

4.1.1(h) Antibody structure

• Globulin protein (immunoglobulin) with quaternary structure.
• Four polypeptides: two heavy, two light, joined by disulfide bridges.
• Y shape, with a flexible hinge region.
• Variable region at each arm tip: specific binding site, complementary to one antigen. Two identical sites per molecule.
• Constant region: same within a class, recognised by phagocytes.

Functions: bind antigen, mark pathogens for phagocytes, clump pathogens, neutralise toxins.

  binding site        binding site
      \                  /
   light chain      light chain
       \    heavy chain /     <- variable regions at the tips
        \______  ______/
               \/   hinge region
               ||    constant region (stem)

Memory hook: the shape of the tip fits the antigen, the same way a substrate fits an active site.

4.1.1(i) Opsonins, agglutinins, anti-toxins

Type	Action	Result
Opsonin	Coats pathogen surface	Phagocyte binds and engulfs more easily
Agglutinin	Links pathogens through two binding sites	Clumps, easier to engulf, less spread
Anti-toxin	Binds toxin	Toxin cannot bind to its target cell

4.1.1(j) Immunity types

	Active	Passive
Natural	Infection and recovery	Placenta; breast milk
Artificial	Vaccination	Injected antibodies (antivenom, tetanus immunoglobulin)

Feature	Active	Passive
Onset	Slow	Immediate
Length	Long, memory cells	Short, antibodies broken down
Own antibody production	Yes	No
Memory cells	Yes	No

4.1.1(k) Autoimmune disease

• The immune system attacks the body’s own cells and tissues, because self and non-self are not distinguished.
• Example: rheumatoid arthritis, where joint tissues are attacked, causing inflammation, pain and cartilage damage.
• Treatment can suppress immunity, which raises infection risk.

4.1.1(l) Vaccination

• Vaccine: antigen from a pathogen in a safe form (weakened, killed, harmless toxin or purified protein).
• Gives artificial active immunity. Primary response forms memory cells, so a real infection gives a secondary response.
• Boosters raise memory cell numbers.
• Herd immunity: so many are immune that spread is limited. It protects those who cannot be vaccinated.
• Simple model: proportion immune needed = 1 - 1/R₀.

R₀	Proportion immune needed
2	50 %
4	75 %
5	80 %
10	90 %

Worked reminder: coverage

R₀ = 4 and the vaccine protects 90 % of those vaccinated.

Immune needed = 1 - 1/4 = 75 %
Coverage = 75 / 0.90 = 83.3 %

Worked reminder: efficacy

A trial has 2000 vaccinated and 2000 placebo participants. There are 6 cases among the vaccinated and 80 among the placebo group.

Reduction = (80 - 6) / 80 x 100 = 92.5 %

Method: explaining a vaccination question

1. Say what the vaccine contains (an antigen, not a live disease-causing pathogen).
2. Describe the primary response and the memory cells it leaves.
3. Describe the secondary response on real infection: faster, larger, no illness.
4. If asked about a population, add herd immunity and what happens when coverage falls.

Why programmes change

• Pathogen changes (influenza surface antigens vary), so vaccines are updated.
• New pathogens appear, so new vaccines are made.
• Disease eradicated (smallpox), so routine vaccination stops.
• Falling uptake allows outbreaks.
• Global issues: cost, storage and transport, conflict, travel.

Routine vaccinations: for example measles, mumps, rubella, diphtheria, tetanus, whooping cough, polio.

4.1.1(m) Medicines

Source	Example
Plants	Aspirin (from salicin in willow bark), digoxin (foxglove)
Microorganisms	Penicillin (fungus Penicillium), antibiotics from Streptomyces bacteria

• Unstudied species may hold useful chemicals, so biodiversity must be maintained.
• Personalised medicine: drug and dose chosen using a person’s genome. Better effect, fewer side effects. Costs, access and data privacy are limits.

4.1.1(n) Antibiotics

Benefits	Risks
Treat bacterial infection	Allergic reactions
Reduce deaths from infection	Side effects
Make surgery and chemotherapy safer	Harm to gut bacteria
	Resistance

Resistance sequence: random mutation, antibiotic as selection pressure, survival and reproduction of resistant bacteria, resistance alleles passed on (including on plasmids), resistant population grows.

Implications: harder-to-treat infections (MRSA), longer illness, higher cost, need for new drugs.

Antibiotics do not work against viruses.

Worked reminder: growth

50 resistant bacteria double every 30 minutes for 5 hours.

Doublings = 10
Number = 50 x 2^10 = 51 200

Command words and data

• Outline: give the main points briefly, with no detail of mechanism.
• Explain: give a reason, so use “because” and name the structure or cell.
• Evaluate: weigh benefits against risks, then give a conclusion.
• Suggest: use your knowledge in a new context, such as a new pathogen or a graph you have not met.

Percentage change = (new - old) / old x 100. Fold change = larger / smaller. When two groups are compared, quote values with units from both, then calculate.

Must-know distinctions

• Plasma cell and B memory cell: one secretes antibody now, one waits.
• T helper and T killer: one signals, one destroys.
• Active and passive: who made the antibody.
• Natural and artificial: everyday life or medical procedure.
• Antibody and antigen: antibody is made by the host, antigen is on the pathogen.

Quick self-test

1. Name the cells that release cytokines in the specific response.
2. Why are plasma cells rich in rough endoplasmic reticulum?
3. Give two reasons the secondary response is faster.
4. How many binding sites has one antibody molecule?
5. What do opsonins do?
6. Is antivenom artificial active or artificial passive immunity?
7. What is an autoimmune disease?
8. R₀ = 5. What proportion must be immune for herd immunity?
9. Give one plant source and one microbial source of a medicine.
10. Why are antibiotics not given for influenza?

Answers

1. T helper cells.
2. They make and secrete large amounts of antibody, which is a protein.
3. Memory cells are already selected and are many in number, and they need a smaller dose of antigen.
4. Two.
5. They bind to pathogens and make phagocytosis easier.
6. Artificial passive.
7. The immune system attacks the body’s own tissues.
8. 1 - 1/5 = 0.8, so 80 %.
9. Foxglove (digoxin); Penicillium (penicillin).
10. The cause is a virus, and antibiotics target bacteria only.

Where marks are usually lost

• Writing “the antibody is complementary to the pathogen” instead of “to the antigen”.
• Saying T cells “make antibodies”.
• Not linking a faster secondary response to memory cells.
• Calling a vaccine “passive”.
• Forgetting units or the time interval when calculating a rate from a graph.
• Saying bacteria “build up resistance” instead of describing mutation and selection.
• Describing herd immunity without saying it protects those not immune.
• Answering a “risk” question about antibiotics with only the benefits.

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).