OxfordAQA International AS and A-level Biology: Immunity and vaccination (9610) – Revision Notes

These revision notes condense section 3.2.5 (3.2.5.1 to 3.2.5.3, the defensive functions of mammalian blood) of the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1, for International AS exams from May/June 2017 and International A-level exams from May/June 2018. For full explanations, read the study guide, then test yourself with the practice questions. Track coverage on the course hub and the printable checklist, and the free diagnostics to spot gaps. Related: causes of disease.

Key definitions

Term	Definition to learn
Antigen	A molecule, usually a protein, that the immune system recognises as foreign and that triggers an immune response
Antibody	A protein made by plasma cells that binds specifically to one antigen
Antigen-presenting cell	A cell that displays foreign antigens on its surface so T cells can recognise them
Antigen-antibody complex	The antibody bound to its complementary antigen
Plasma cell	Descendant of an activated B cell that secretes antibody
Memory cell	A persistent cell giving a fast, large response on re-exposure
Vaccine	A preparation of antigens that triggers memory cell production without causing the disease
Herd immunity	Indirect protection of non-immune people when enough of the population is immune to stop transmission

3.2.5.1 Principles of immunology

• Surface molecules (many are proteins) identify a cell. The immune system uses them to spot pathogens, toxins, cells from another individual of the same species and abnormal body cells.
• Antigen variability: if antigens change, memory cells no longer match. Disease: reinfection with a new strain. Prevention: vaccines must be updated, or are hard to make.
• T cells: cell-mediated immunity. B cells: humoral immunity, meaning antibodies in body fluids.

Phagocytosis in steps

1. Attracted to pathogen; receptors bind it
2. Membrane engulfs it -> phagosome
3. Lysosomes fuse with phagosome
4. Hydrolytic enzymes digest the pathogen
5. Antigens may be displayed on the phagocyte surface

3.2.5.2 B cell response

Method in steps

Macrophage engulfs and presents antigen
-> T cell carrying complementary receptor attaches, is activated
-> B cell with complementary surface antibody binds antigen
-> B cell clones by mitosis (clonal expansion)
-> plasma cells secrete antibody; memory cells persist

Antibody structure checklist

Feature	Detail
Chains	2 heavy + 2 light polypeptides
Bonds between chains	Disulfide bridges
Variable region	Forms two identical antigen-binding sites; sequence differs between antibodies
Constant region	Same within a class of antibody
Hinge	Gives flexibility

Destroying bacteria (limited to two mechanisms)

• Agglutination: one antibody can join two cells because it has two binding sites, so bacteria clump.
• Phagocytosis: phagocytes engulf antibody-coated bacteria; lysosomes digest them.

3.2.5.3 Vaccination

	Primary response	Secondary response
Lag before antibody rises	Long	Short
Rate of rise	Slow	Fast
Peak concentration	Low	High
Duration	Shorter	Longer
Cause	Few B cells fit; clone must form	Memory cells already present

Active against passive

	Active	Passive
Natural	Catching the disease	Antibodies via placenta or breast milk
Artificial	Vaccination	Injection of ready-made antibodies
Memory cells	Yes	No
Lasts	Years	Weeks to months

Herd immunity reminders

• It protects those who cannot be vaccinated, such as very young babies.
• It weakens if coverage falls, if the vaccine is less effective, or if antigens change.
• Simple model: minimum immune fraction = 1 - 1/R. Divide by vaccine efficacy to get coverage needed.

Calculation toolkit

Quantity	Method
Attack rate	cases / participants x 100
Vaccine efficacy	(attack rate in placebo - attack rate in vaccine) / attack rate in placebo x 100
Fold increase	later value / earlier value
Magnification	image size / actual size (same units)
Percentage change	(new - old) / old x 100

Worked reminder: 4 cases among 5,000 vaccinated and 40 among 5,000 on placebo gives attack rates of 0.08% and 0.8%, so efficacy = (0.8 - 0.08) / 0.8 x 100 = 90%.

Model explanations to learn

These are the linked chains of reasoning that long answers need. Learn the order, not the exact wording.

Why the secondary response is faster and larger

1. The first exposure produced memory cells specific to that antigen.
2. On re-exposure, many memory cells recognise the antigen at once, so no search for a matching cell is needed.
3. They divide rapidly by mitosis and form plasma cells.
4. More plasma cells secrete more antibody sooner, so the peak is higher and symptoms are usually avoided.

Why a vaccine protects

1. It supplies the antigen without causing the disease.
2. The antigen is presented, T cells and B cells with matching receptors are selected, and clones form.
3. Plasma cells make antibody (primary response) and memory cells remain.
4. Later infection by the real pathogen triggers a secondary response, so the pathogen is cleared before it multiplies enough to cause illness.

Why antibodies are specific

• The variable region has a particular sequence of amino acids, so its tertiary structure forms a binding site with a particular shape.
• Only an antigen with a complementary shape fits.
• Different B cells make antibodies with different variable regions, so a huge range of antigens can be recognised.

Why the immune response begins slowly

• Only a few B cells and T cells carry receptors for any one antigen.
• They must be selected and must divide before enough plasma cells exist to make a difference.
• During this lag, a person may show symptoms, and non-specific defences such as phagocytosis have to cope alone.

Reading a vaccine data question

Work through the same four moves each time.

1. Read the axes or column headings. Note units and whether numbers are counts or percentages.
2. Quote figures. Give values from the table or graph, with units, and a calculated difference or ratio.
3. Compare like with like. Use attack rates rather than raw case numbers when group sizes differ.
4. Qualify the conclusion. Mention sample size, duration, and what the data cannot show, for example protection after several years.

A sentence frame that works for evaluation: “The vaccine reduced cases from X% to Y%, which is a Z% reduction, but the trial only followed participants for N months, so long-term protection is not shown.”

Evaluating vaccine trials

• Was there a control group, random allocation and double-blinding?
• Is the sample large and representative of the people who will receive the vaccine?
• Was the outcome antibody concentration or actual disease? Disease is stronger evidence of protection.
• How long were participants followed up?
• Were side effects compared between groups?
• Is the difference statistically significant, and could another factor explain it?

Must-know distinctions

• Antigen or antibody: antigens trigger; antibodies bind.
• Vaccine or serum: a vaccine gives antigens (active); injected antibodies give passive immunity.
• Plasma cell or memory cell: plasma cells secrete now; memory cells wait.
• Cell-mediated or humoral: T cell actions or antibodies from B cells.

Quick self-test

1. State what is meant by an antigen.
2. Name the organelle that releases digestive enzymes into a phagosome.
3. How many polypeptide chains make up an antibody, and how are they held together?
4. Explain why an antibody with two binding sites can cause agglutination.
5. A secondary response peaks at 200 units and the primary at 8 units. Calculate the fold increase.
6. For the same data, calculate the percentage increase.
7. Calculate the minimum immune fraction needed for herd immunity when R = 4.
8. Why does a baby receiving antibodies in breast milk not develop memory cells?
9. A micrograph of a phagocyte is 40 mm across at magnification x5000. Calculate the actual diameter in micrometres.
10. Why might a vaccine against a variable virus need to be given again each year?

Answers

1. A molecule, usually a protein, recognised as foreign that triggers an immune response.
2. Lysosome.
3. Four (two heavy, two light), held together by disulfide bridges.
4. Each antibody can bind two bacterial cells, so many antibodies link many cells into clumps.
5. 200 / 8 = 25-fold.
6. (200 - 8) / 8 x 100 = 2,400%.
7. 1 - 1/4 = 0.75, so 75%.
8. The baby’s own B cells have not met the antigen, so no clones or memory cells form.
9. 40 / 5000 = 0.008 mm = 8 micrometres.
10. The virus’s antigens change, so memory cells from the old vaccine may not recognise the new strain.

Where marks are usually lost

• Defining an antigen as “something that causes disease” instead of a molecule that triggers an immune response.
• Saying antibodies “fit” without stating that the variable region has a binding site complementary to the antigen.
• Describing agglutination without stating that each antibody has two binding sites.
• Leaving out lysosomes when describing digestion in phagocytosis.
• Writing that memory cells produce antibodies straight away, instead of dividing into plasma cells.
• Treating herd immunity as 100% immunity.
• Calling a trial reliable without mentioning sample size, a control group or blinding.
• Giving efficacy as the vaccinated attack rate, instead of the reduction relative to placebo.

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.