Cell Recognition and the Immune System: AQA A Level Biology Exam Questions by Topic

AQACell Recognition and the Immune SystemExam Questions
Written by Tom Whitburn

Cell recognition and the immune system (AQA 3.2.4) is one of the biggest Year 12 topics, and it turns up on almost every paper, often in an unfamiliar context such as snake antivenom, a cancer drug or a test for Lyme disease. You need to know how antigens let the immune system recognise pathogens, other people's cells, abnormal cells and toxins; phagocytosis; the cellular response with antigen-presenting cells and helper T cells; the humoral response with B cells, plasma cells, memory cells and antibodies; vaccines, herd immunity and active v passive immunity; HIV and AIDS; and how monoclonal antibodies are used in treatment, diagnosis and the ELISA test.

The examiners' reports show the same slips every year. Students name B and T cells when asked which cells trigger a response, confuse lysosomes with lysozymes, give antibodies an 'active site', say B cells rather than plasma cells release antibodies, claim herd immunity protects against tetanus, and give HIV a cell wall or DNA.

Start with cell recognition and phagocytosis, then T cells, B cells and antibodies, then vaccines and HIV, and finish with monoclonal antibodies, ELISA and an evaluation question. Answer each on paper before you open the mark scheme. If you'd like help with this topic, my AQA masterclasses run online on Tuesdays at 5.15pm for Year 12 and on Wednesdays or Thursdays at 6.30pm for Year 13.

What you need from GCSE and Year 12

Each question on this page assumes you're secure on these GCSE and Year 12 ideas. If any of them feels shaky, revise it before you start.

  • GCSE: white blood cells defend the body by phagocytosis, by producing antibodies and by producing antitoxins.
  • GCSE: vaccines contain dead or inactive pathogens; they stimulate white blood cells to make antibodies, so a later infection is fought off quickly.
  • GCSE: antibiotics kill bacteria but not viruses; HIV attacks the immune system and can lead to AIDS.
  • Year 12 (AQA 3.1.4.1): proteins have a specific tertiary and quaternary structure, held by bonds such as disulfide bridges. See the Proteins page.
  • Year 12 (AQA 3.2.1.2): the structure of viruses: genetic material, capsid and attachment proteins. See the Prokaryotic Cells and Viruses page.

Key terms

These words come up in the questions and mark schemes. Examiners expect you to use them exactly.

  • Antigen: a foreign protein (or other molecule) that stimulates an immune response leading to the production of antibodies.
  • Antibody: a protein with two identical antigen-binding sites that are complementary to one specific antigen; made by plasma cells.
  • Phagocytosis: engulfing a pathogen into a phagosome, which fuses with a lysosome so lysozymes hydrolyse the pathogen.
  • Antigen-presenting cell: a cell, such as a phagocyte, that displays foreign antigens on its cell-surface membrane.
  • Helper T cell (TH cell): a T cell with a receptor complementary to the presented antigen; it stimulates cytotoxic T cells, B cells and phagocytes.
  • Clonal selection: the B cell with antibodies complementary to the antigen is stimulated to divide by mitosis, forming a clone.
  • Plasma cells and memory cells: cells formed from the B cell clone: plasma cells secrete antibodies; memory cells stay in the blood and give a faster, larger secondary response.
  • Agglutination: antibodies binding to antigens on several bacteria, clumping them together so phagocytes can engulf them.
  • Active and passive immunity: active: your own plasma cells make antibodies and memory cells form (long-lasting, slow to start); passive: antibodies are given from outside (immediate, short-lived, no memory cells).
  • Herd immunity: when so many people are vaccinated that a pathogen can't spread, protecting unvaccinated people too.
  • Monoclonal antibody: antibodies with the same tertiary structure, made by a clone of identical plasma cells, used to target drugs, in diagnosis and in ELISA.

What these questions cover (AQA 3.2.4)

The questions test these statements from the AQA AS and A-level Biology specification (7401/7402):

  • Cell recognition: 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.
  • Antigens: Definition of antigen. The effect of antigen variability on disease and disease prevention.
  • Phagocytosis: Phagocytosis of pathogens. The subsequent destruction of ingested pathogens by lysozymes.
  • The cellular response: The response of T lymphocytes to a foreign antigen (the cellular response).
  • The cellular response: The role of antigen-presenting cells in the cellular response.
  • The cellular response: The role of helper T cells (TH cells) in stimulating cytotoxic T cells (TC cells), B cells and phagocytes. The role of other T cells is not required.
  • The humoral response: The response of B lymphocytes to a foreign antigen, clonal selection and the release of monoclonal antibodies (the humoral response).
  • The humoral response: Definition of antibody.
  • The humoral response: Antibody structure.
  • The humoral response: The formation of an antigen-antibody complex, leading to the destruction of the antigen, limited to agglutination and phagocytosis of bacterial cells.
  • The humoral response: The roles of plasma cells and of memory cells in producing primary and secondary immune responses.
  • Vaccines and immunity: The use of vaccines to provide protection for individuals and populations against disease. The concept of herd immunity.
  • Vaccines and immunity: The differences between active and passive immunity.
  • HIV: Structure of the human immunodeficiency virus (HIV) and its replication in helper T cells.
  • HIV: How HIV causes the symptoms of AIDS. Why antibiotics are ineffective against viruses.
  • The use of monoclonal antibodies in: targeting medication to specific cell types by attaching a therapeutic drug to an antibody
  • The use of monoclonal antibodies in: medical diagnosis. (the specification adds that details of the commercial or scientific production of monoclonal antibodies are not required)
  • Ethics: Ethical issues associated with the use of vaccines and monoclonal antibodies.
  • ELISA: The use of antibodies in the ELISA test.
  • Students should be able to discuss ethical issues associated with the use of vaccines and monoclonal antibodies
  • Students should be able to evaluate methodology, evidence and data relating to the use of vaccines and monoclonal antibodies.

How to use this page

Write your answer on paper before you open the mark scheme. Allow about 1.3 minutes per mark: the 18 questions are worth 47 marks, so about 61 minutes in total. Then mark your answer strictly against the mark scheme and read the examiners' tip underneath it. If you'd rather print the questions, download the PDF pack.

Cell recognition and antigens (3.2.4)

Question 1

A level Paper 3 · June 2024 · Q01.1 · 3 marks · Easy

Fill six gaps in a passage about cell surface molecules, antibodies, plasma cells and immunity.

Question text: a passage with six numbered gaps: each type of cell has specific molecules on its (1) that identify it; an antibody is a (2) with two (3) binding sites; antibodies are made and released by (4) cells; the response to a vaccine is an example of (5) immunity; (6) immunity occurs when a large proportion of a population becomes immune, 3 marks.
Show the mark scheme Mark scheme: 1 cell-surface membrane; 2 protein; 3 antigen; 4 plasma; 5 active; 6 herd. Six correct for 3 marks, 4–5 for 2, 2–3 for 1.

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From the examiners' report: A quarter got all three marks. The usual slips were writing just 'surface' instead of cell-surface membrane, 'B cell' instead of plasma cells, and 'passive' for the response to a vaccine.

Question 2

A level Paper 3 · June 2023 · Q06.1 · 2 marks · Hard

Give two types of cell that can stimulate an immune response.

Question text: give two types of cell that can stimulate an immune response, 2 marks.
Show the mark scheme Mark scheme: any two of pathogens (or cells from a different species); cells from other organisms of the same species; abnormal body cells, such as cancer cells or virus-infected cells; antigen-presenting cells. Reject toxins; ignore B cells and T cells.

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From the examiners' report: Just over half scored nothing because they named B cells and T cells, the cells that respond. The question wants cells that trigger a response: pathogens, cells from another person (a transplant) and abnormal or cancer cells.

Phagocytosis and the cellular response (3.2.4)

Question 3

AS Paper 1 · November 2020 · Q03.1 · 3 marks

Describe how a phagocyte destroys a pathogen in the blood.

Question text: describe how a phagocyte destroys a pathogen present in the blood, 3 marks.
Show the mark scheme Mark scheme: engulfs (endocytosis); forming a vesicle or phagosome, which fuses with a lysosome; enzymes (lysozymes) digest or hydrolyse the pathogen.

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From the examiners' report: Use the right terms in order: the pathogen is engulfed into a phagosome (a vesicle, not a vacuole), a lysosome fuses with it, and lysozymes hydrolyse the pathogen. Don't mix up lysosomes and lysozymes.

Question 4

AS Paper 1 · June 2018 · Q10.1 · 3 marks · Medium

Use a passage on Crohn's disease to suggest how bacteria trigger swelling of the intestine lining.

Passage about Crohn's disease: normal intestinal bacteria are controlled by T cells made slowly and in small numbers, which don't survive long, so release little cytokine; cytokines cause swelling of the intestine lining; Crohn's disease may be triggered by pathogenic bacteria causing an unusually large T cell response. Question 10.1: suggest how pathogenic bacteria could trigger swelling (lines 6–10), 3 marks.
Show the mark scheme Mark scheme, any three: antigen of the pathogenic bacteria; causes more or faster T cell production; against the pathogen and normal bacteria; the T cells live longer; more cytokines causing swelling are produced.

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From the examiners' report: 70.7% scored at least one mark. Start with the antigen on the bacteria, then more T cells, then more cytokines from the passage: it's the cytokines, not a build-up of T cells or water, that cause the swelling.

B cells, antibodies and the humoral response (3.2.4)

Question 5

AS Paper 1 · June 2016 · Q07.1 · 4 marks

Describe how the HPV vaccine leads to the production of antibody against HPV.

Question text: human papilloma virus (HPV) is the main cause of cervical cancer and a vaccine has been developed; describe how giving this vaccine leads to production of antibody against HPV, 4 marks.
Show the mark scheme Mark scheme, any four: the vaccine contains HPV antigen; displayed on antigen-presenting cells; a specific helper T cell stimulates a specific B cell; the B cell divides by mitosis to form a clone of plasma cells; plasma cells produce antibody.

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From the examiners' report: There's no examiners' report for this paper, so this tip comes from the mark scheme. Give the full sequence: antigen, antigen-presenting cell, specific helper T cell, specific B cell, mitosis to make plasma cells, antibody.

Question 6

A level Paper 3 · November 2020 · Q03.4 · 3 marks · Medium

Describe how a frog's B lymphocytes would respond to vaccination against Ranavirus.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Introduction: in Europe, closely related Ranaviruses have infected many frog species. Question: describe how the B lymphocytes of a frog would respond to vaccination against Ranavirus, assuming they respond like human B lymphocytes; do not include the cellular response, 3 marks.
Show the mark scheme Mark scheme, any three: a B cell with a complementary receptor binds to the viral antigen; the B cell divides by mitosis (clones); plasma cells release antibodies; memory cells are produced.

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From the examiners' report: 37% got all three. Name plasma cells (not 'B cells') as the antibody makers, and B cells aren't macrophages. Most answers lost time describing T cells even though the question said not to.

Question 7

AS Paper 1 · June 2024 · Q07.1 · 2 marks

Draw a monoclonal antibody attached to a drug and label one structural feature.

Question text: a drug is delivered to diseased body cells by a monoclonal antibody attached to it, an antibody–drug complex (ADC). Figure 8 shows a small rectangle labelled Drug; complete the figure to show the antibody attached and label one structural feature, 2 marks.
Show the mark scheme Mark scheme: a Y-shaped antibody joined to the drug with the arms of the Y left free; one label from disulfide bridge, antigen-binding site, variable region, constant region, light chain, heavy chain, hinge region or polypeptide.

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From the examiners' report: A plain Y wasn't enough: draw the two heavy and two light chains. Most attached the drug to an arm (the variable region), which is wrong; it goes on the constant region so the binding sites stay free. There's no active site or receptor to label.

Question 8

AS Paper 2 · June 2019 · Q04.1 · 2 marks

Describe and explain how antibodies stimulate phagocytosis.

Question text: describe and explain the role of antibodies in stimulating phagocytosis; do not include details of the process of phagocytosis, 2 marks.
Show the mark scheme Mark scheme: antibodies bind to antigens (form antigen-antibody complexes) or act as markers; they cause clumping (agglutination) or attract phagocytes. Reject clotting.

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From the examiners' report: Antibodies bind to antigens to form antigen-antibody complexes, which clump the bacteria together (agglutination) and attract phagocytes. 'Signal', 'alert' or 'identify' didn't score, and antibodies have binding sites, not active sites.

Vaccines, immunity and antigen variability (3.2.4)

Question 9

A level Paper 1 · June 2018 · Q07.1 · 2 marks

Explain how antivenom works and why passive, not active, immunity is needed.

Question text: a venomous snake injects a toxin; antivenom containing antibodies against the toxin is injected as treatment, an example of passive immunity. Explain how antivenom works and why passive immunity is essential rather than active immunity, 2 marks.
Show the mark scheme Mark scheme: antibodies bind to the toxin (antigen) and cause its destruction, for example by agglutination or phagocytosis; active immunity would be too slow. Ignore neutralising; reject killing the toxin; 'passive is fast' alone isn't enough.

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From the examiners' report: Only 28.1% got both marks. Say the antibodies bind to the toxin and lead to its destruction, then compare: active immunity would be too slow. Antivenom isn't a vaccine and doesn't trigger an immune response.

Question 10

AS Paper 1 · June 2022 · Q09.3 · 2 marks · Hard

Suggest how vaccinating as many babies as possible protects the population against measles and tetanus.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Passage: IgG antibodies cross the placenta; the UK vaccinates as many babies as possible against measles viruses and tetanus bacteria; measles spreads quickly from infected people; tetanus bacteria enter through skin wounds and don't spread from person to person; children get three tetanus vaccinations. Question 09.3: suggest how vaccinating babies protects the population against measles and against tetanus (lines 9–11), 2 marks.
Show the mark scheme Mark scheme: measles, herd immunity reduces spread; tetanus, no herd immunity, it only protects the individual, or skin wounds are common in children.

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From the examiners' report: Only 42% scored. For measles say herd immunity reduces the spread. Tetanus doesn't spread between people, so there's no herd immunity: each vaccinated child is protected individually.

Question 11

AS Paper 1 · June 2022 · Q09.5 · 2 marks · Medium

Explain why more than one tetanus vaccination gives good immunity.

Question text: explain why giving children more than one tetanus vaccination develops good immunity against tetanus (lines 15–17), 2 marks.
Show the mark scheme Mark scheme: more memory cells are produced; so a higher concentration of antibodies, or more rapid production of antibodies on further infection.

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From the examiners' report: 'A stronger' or 'faster immune response' isn't enough. Say each dose makes more memory cells, so antibodies are made faster and in higher concentration if tetanus bacteria get in.

Question 12

A level Paper 3 · June 2024 · Q01.2 · 1 mark · Medium

Suggest one reason why there is no effective vaccine for HIV.

Question text: there is currently no effective vaccine available for HIV; suggest one reason why, 1 mark.
Show the mark scheme Mark scheme, any one: high rate of mutation; high genetic diversity; HIV in cells could still spread infection; HIV DNA inserts itself into host DNA; lack of funding; HIV reduces T cells so there is no immune response to the vaccine. Accept antigenic variability.

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From the examiners' report: Just under half scored, mostly for antigenic variability: HIV mutates so often that its antigens change shape. Don't confuse vaccines with antibiotics by saying HIV has no cell wall.

HIV and AIDS (3.2.4)

Question 13

A level Paper 3 · June 2024 · Q01.3 · 2 marks · Easy

Use a table of antibiotic actions to explain why ciprofloxacin and penicillin don't work against HIV.

Table 1: ciprofloxacin causes double-stranded DNA to break apart; penicillin prevents formation of crosslinks between murein chains. Question: explain why each antibiotic is not effective against HIV, 2 marks.
Show the mark scheme Mark scheme: ciprofloxacin, HIV has RNA, not DNA; penicillin, HIV has no cell wall or murein. Reject single-stranded DNA and wrong viral structures such as a cell membrane or a chitin cell wall.

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From the examiners' report: Just over half got both marks. HIV's genetic material is RNA, not single-stranded DNA, and it has no cell wall of any kind, so don't give it a chitin wall or a cell membrane.

Question 14

A level Paper 3 · November 2021 · Q02.1 · 4 marks · Medium

Describe how HIV is replicated once inside a helper T cell.

Question text: describe how the human immunodeficiency virus (HIV) is replicated once inside helper T cells (TH cells), 4 marks.
Show the mark scheme Mark scheme: RNA is converted into DNA by reverse transcriptase; the DNA is inserted into the helper T cell's DNA; the DNA is transcribed into HIV mRNA; the mRNA is translated into new viral proteins for assembly into virus particles.

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From the examiners' report: Only 1.89% got full marks. Avoid vague phrases like 'uses the cell's machinery': name reverse transcriptase, insertion into the T cell's DNA, transcription to mRNA and translation into viral proteins.

Question 15

AS Paper 2 · June 2025 · Q08.1 · 3 marks · Medium

Use HIV and helper T cell counts to explain why other infections are likely after 11 years.

Table 4: HIV RNA particles per cm³ of blood and helper T cell count per mm³ over 12 years in an untreated person: T cells fall from 1000 at infection to 597 at 10 years, 150 at 11 years and 5 at 12 years, while HIV particles rise to 135 000. Question: explain why other infections are more likely after 11 years, 3 marks.
Show the mark scheme Mark scheme: after 11 years there is a large decrease in, or very few, helper T cells; so fewer B cells divide by mitosis or undergo clonal selection; so fewer plasma cells produce antibodies.

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From the examiners' report: Under 5% got all three. Don't just quote 150 or 5: say the helper T cell count has fallen to a very low level, then that fewer B cells divide (clonal selection) and fewer plasma cells make antibodies.

Monoclonal antibodies and ELISA (3.2.4)

Question 16

AS Paper 2 · June 2022 · Q03.3 · 3 marks · Hard

Suggest how an anti-ZO-1 monoclonal antibody helped a scientist identify ileum cells.

Information from earlier in this question:

Earlier part of the same exam question, giving the information this part uses. Introduction: Figure 1, image of an ileum cell with microvilli. Question: the protein ZO-1 is found on the surface of ileum cells; a scientist used an anti-ZO-1 monoclonal antibody to identify ileum cells with an optical microscope; suggest how, 3 marks.
Show the mark scheme Mark scheme, any three: ZO-1 is in the cell-surface membrane; the antibody is complementary to ZO-1; so it binds to ZO-1 (antigen-antibody complex); a dye, stain or fluorescent marker is attached to the antibody. Reject active site.

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From the examiners' report: Only 8% got full marks. Say the antibody is complementary to ZO-1 so it binds to it, and that it carries a dye or fluorescent marker you can see. 'Colour' or 'marker' on its own isn't enough, and there's no active site.

Question 17

AS Paper 2 · June 2024 · Q08.1 · 2 marks · Hard

Explain why failing to wash the well in an ELISA test for Lyme disease can give a false positive.

Figure 5: ELISA steps for antibodies to Borrelia burgdorferi: 1 antigens attached to a well; 2 blood added, any antibodies bind; 3 well washed, a second antibody with an enzyme attached is added that binds to those antibodies; 4 well washed again and substrate added, which the enzyme converts to a coloured product. Question 08.1: failure to wash the well in step 4 can give a false positive; explain why, 2 marks.
Show the mark scheme Mark scheme: the second antibody with the enzyme remains in the well; so the substrate is converted to a coloured product.

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From the examiners' report: Stick to the steps: unbound second antibody with its enzyme is left behind, so it turns the substrate into the coloured product even with no Lyme antibodies present. It's nothing to do with contamination by other bacteria.

Evaluating vaccine use (3.2.4)

Question 18

AS Paper 1 · June 2023 · Q06.4 · 4 marks · Hard

Evaluate whether 10- to 12-year-old boys should be given the HPV vaccine.

Question text: HPV is transmitted through sexual contact; more than 95% of cervical cancers (which only affect females) are due to HPV; HPV infection of other tissues raises cancer risk but rarely; the vaccine is over 80% effective if given before exposure; there is herd immunity when over 50% are vaccinated. Evaluate whether 10- to 12-year-old boys should be given the vaccine, 4 marks.
Show the mark scheme Mark scheme, max 3 for: given before exposure; reduces transmission to girls; boys can be infected; needed to reach herd immunity (over 50%); boys have some increased cancer risk. Against: boys are at less risk than females, or cervical cancer only affects females; possible side effects. 4 max.

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From the examiners' report: Give both sides and use the figures: vaccinating before sexual activity, cutting transmission to girls and reaching the 50% for herd immunity, against a lower cancer risk for boys and possible side effects. 'Not 100% effective' isn't a reason to refuse it.

Where students lose marks (from AQA examiners' reports and mark schemes)

Each point below is followed by wording that gained marks.

  • Cells that trigger a response, not cells that respond: Just over half scored nothing for two types of cell that stimulate an immune response because they named B cells and T cells. In an earlier paper, many named pathogens when the question excluded them.

    ✔ Gains credit: "Pathogens; cells from other organisms of the same species; abnormal body cells (cancer cells)" and "(cells from) other organisms/transplants; abnormal/cancer cells; cells infected by virus".

  • Lysosomes fuse, lysozymes digest: Examiners asked for correct terms in phagocytosis: some wrote of vacuoles rather than vesicles, or confused lysosomes with lysozymes.

    ✔ Gains credit: "Engulfs; forming a vesicle/phagosome which fuses with a lysosome; enzymes (lysozymes) digest/hydrolyse."

  • Antibodies have binding sites, not active sites: References to an antibody's 'active site' lost marks across several questions, and 'signal', 'identify' or 'alert' phagocytes gained nothing. Only 8% got full marks for the ZO-1 monoclonal antibody question.

    ✔ Gains credit: "Bind to antigen/form antigen-antibody complexes; cause clumping/agglutination; attract phagocytes" and "antibody is complementary to ZO-1, so binds to it".

  • Plasma cells make the antibodies: In the gap-fill passage, 'B cell' was a common wrong answer for the cells that make and release antibodies, and in the Ranavirus question errors included not naming plasma cells.

    ✔ Gains credit: "Plasma (cells)" and "B cell divides by mitosis; plasma cells release antibodies; memory cells."

  • Passive immunity is faster, so say it: Only 28.1% explained antivenom fully. Some described binding without destruction, some wrote 'complementary' instead of binding, some said active immunity just 'takes time', and some treated antivenom as a vaccine.

    ✔ Gains credit: "Antibodies bind to the toxin and cause its destruction; active immunity would be too slow."

  • No herd immunity against tetanus: Only 42% scored on vaccinating babies. Many claimed herd immunity for tetanus, which doesn't spread between people, or explained how vaccines work in general.

    ✔ Gains credit: "Measles: herd immunity reduces spread. Tetanus: no herd immunity; it only protects the individual."

  • More doses, more memory cells: For several tetanus doses, answers about a 'stronger' or 'faster immune response' lacked the detail of memory cells and antibodies.

    ✔ Gains credit: "More memory cells; so a higher concentration/more rapid production of antibodies."

  • HIV has RNA and no cell wall: Just over half explained why two antibiotics don't affect HIV. Errors included HIV having single-stranded DNA, a chitin cell wall or a cell membrane. In another paper only a quarter said why antibiotics don't work on viruses; many said viruses 'hide inside cells'.

    ✔ Gains credit: "(HIV) has RNA, not DNA; (HIV) has no cell wall/does not contain murein."

Download the questions

Download the PDF pack (18 questions, mark schemes at the end)

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Questions, mark schemes and examiners' report extracts © AQA.

Tom Whitburn
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