Immunity & Disease
12 free practice questions with explanations
PassNova has 12 free A-level Biology practice questions on Immunity & Disease, each with a clear explanation. Practise them in the browser with instant feedback — 100% free, no sign-up, on any device. Updated for 2026.
Immunity & Disease: example questions & answers
12 worked examples with answers and explanations below. Practise them in the browser with instant feedback on every answer.
What is an antigen, in the context of the specific immune response?
- AAny protein produced by a B lymphocyte that binds a pathogen
- BA molecule, usually on a cell surface, that is recognised as foreign and triggers an immune response✓
- CA chemical released by mast cells that causes inflammation
- DA signalling molecule that activates T helper cells only
Answer: An antigen is a molecule (often a cell-surface protein or glycoprotein) recognised as non-self, stimulating the production of antibodies and an immune response. Antibodies are made by plasma cells, not the definition of an antigen.
Place the stages of phagocytosis in the correct order.
- APhagocyte attracted by chemicals → pathogen engulfed forming a phagosome → lysosome fuses and releases hydrolytic enzymes → soluble products absorbed✓
- BLysosome fuses with phagosome → phagocyte engulfs pathogen → enzymes digest pathogen → antigens presented
- CAntibodies digest the pathogen → phagocyte engulfs debris → vesicle forms → antigens displayed
- DPathogen binds MHC → phagosome forms → enzymes released → clonal selection occurs
Answer: A phagocyte is attracted by chemotaxis, engulfs the pathogen into a phagosome (phagocytic vacuole), a lysosome fuses to form a phagolysosome and releases lysozymes/hydrolytic enzymes that digest the pathogen, and soluble products are absorbed.
What is the principal role of a T helper (CD4⁺) cell once activated by an antigen-presenting cell?
- ATo directly destroy infected cells by releasing perforin
- BTo release cytokines (chemical signals) that stimulate B cells, cytotoxic T cells and phagocytes✓
- CTo engulf and digest pathogens by phagocytosis
- DTo secrete large quantities of antibody into the blood
Answer: Activated T helper cells release cytokines (interleukins) that stimulate clonal expansion of B cells into plasma cells, activate cytotoxic T cells, and enhance phagocytosis. Killing infected cells with perforin is the role of cytotoxic T cells.
How does a cytotoxic T (CD8⁺) cell destroy a body cell that is infected with a virus?
- AIt releases perforin, which makes pores in the cell-surface membrane, causing the cell to die✓
- BIt secretes antibodies that agglutinate the virus
- CIt engulfs the infected cell by endocytosis
- DIt releases histamine to trigger inflammation around the cell
Answer: Cytotoxic T cells release the protein perforin, which embeds in the target cell's membrane and forms pores, making it freely permeable so the cell undergoes lysis/apoptosis. This destroys cells harbouring intracellular pathogens such as viruses.
In the humoral response, what is the role of a plasma cell?
- ATo remain in the blood for years and respond rapidly on re-infection
- BTo present antigen to T helper cells
- CTo release cytokines that activate phagocytes
- DTo secrete large amounts of a specific antibody into the blood and lymph✓
Answer: Plasma cells are differentiated B cells that act as antibody factories, secreting thousands of monospecific antibody molecules per second. Long-lived rapid responders are memory cells, a separate B-cell clone product.
The secondary immune response is faster and produces more antibody than the primary response. What is the main reason for this?
- AAntibodies from the primary response are still circulating in large numbers
- BThe pathogen has become weaker after the first infection
- CMemory cells produced in the primary response divide rapidly into plasma cells on re-exposure✓
- DPhagocytes work faster the second time they meet a pathogen
Answer: During the primary response, memory B (and T) cells are formed by clonal selection. On a second encounter with the same antigen, these memory cells divide and differentiate rapidly into plasma cells, giving a quicker, larger, longer-lasting antibody response.
Some antibodies cause pathogens to clump together, making them easier for phagocytes to engulf. This process is called:
- Aopsonisation
- Bagglutination✓
- Cneutralisation
- Dlysis
Answer: Because each antibody has two (or more) binding sites, one antibody can bind antigens on two different pathogens, cross-linking them into clumps. This agglutination immobilises pathogens and increases the rate of phagocytosis.
A person recovers from measles and is immune for life without ever being vaccinated. This is an example of:
- Anatural active immunity✓
- Bartificial active immunity
- Cnatural passive immunity
- Dartificial passive immunity
Answer: Immunity gained by being infected naturally and mounting your own immune response (forming memory cells) is natural active immunity. Vaccination would be artificial active; antibodies received ready-made (e.g. across the placenta or by injection) would be passive.
Herd immunity protects unvaccinated individuals in a population. This works because:
- Avaccinated people produce antibodies that pass to unvaccinated people
- Bthe pathogen mutates into a harmless form once most people are vaccinated
- Ca high proportion of immune individuals reduces transmission, so the pathogen is less likely to reach susceptible people✓
- Dunvaccinated people develop natural immunity from contact with the vaccine
Answer: When a sufficiently high proportion of the population is immune, there are too few susceptible hosts for the pathogen to spread efficiently, so transmission chains break down. This indirectly protects those who are not (or cannot be) vaccinated.
Why is it difficult to develop an effective long-lasting vaccine against the influenza virus?
- AFrequent changes to its surface antigens mean memory cells no longer recognise new strains (antigenic variation)✓
- BThe virus cannot be cultured in the laboratory
- CInfluenza does not produce any antigens
- DThe immune system cannot make memory cells against viruses
Answer: Influenza shows antigenic variation: its surface antigens (haemagglutinin and neuraminidase) change frequently through mutation. Memory cells specific to previous antigens no longer match, so people can be re-infected and vaccines must be updated.
HIV specifically infects and ultimately destroys T helper cells. Why does this lead to AIDS and a wider failure of the immune system?
- AT helper cells are the only cells that perform phagocytosis
- BT helper cells produce all of the body's antibodies
- CWithout T helper cells, B cells and cytotoxic T cells are not properly activated, so specific responses to many pathogens fail✓
- DT helper cells form the physical skin barrier against pathogens
Answer: T helper cells coordinate the immune response by releasing cytokines that activate B cells, cytotoxic T cells and phagocytes. As HIV depletes them, the whole specific response is undermined, leaving the person vulnerable to opportunistic infections (AIDS).
Monoclonal antibodies are described as 'monoclonal'. What does this term indicate?
- AThey are produced by many different B-cell clones
- BThey can bind to any antigen non-specifically
- CThey are identical antibodies derived from a single B-cell clone, all specific to the same antigenic determinant✓
- DThey are antibodies that lack a constant region
Answer: Monoclonal antibodies are produced from a single clone of B cells (typically via hybridoma cells), so every molecule is identical and binds the same specific epitope. This specificity underlies their use in diagnosis and targeted therapy.