Immunity & Disease

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 (such as histamine) in inflammation
• DA signalling molecule released by T helper cells to recruit phagocytes

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 the phagosome → phagocyte engulfs the pathogen → hydrolytic enzymes digest the pathogen → antigens are presented on the cell surface
• CAntibodies secreted by plasma cells digest the pathogen → the phagocyte engulfs the remaining debris → a vesicle forms → antigens are displayed on the membrane
• DPathogen binds MHC → phagosome (vacuole) 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, then break them down using hydrolytic enzymes released from lysosomes
• DTo secrete large quantities of antibody into the blood and lymph, so that free pathogens are agglutinated before phagocytosis

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 particles, clumping them so that phagocytes can engulf several at once
• CIt engulfs the whole infected cell by endocytosis
• DIt releases histamine (a vasodilator) 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 processed antigen on MHC molecules to T helper cells, so that they release cytokines
• CTo release cytokines (interleukins) 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?

• AThe plasma cells formed in the primary response survive indefinitely and keep secreting antibody at the same high rate
• BThe pathogen has become weaker (attenuated) 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 encounter 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, which are then passed on to unvaccinated contacts
• Bthe pathogen mutates into a less harmful form once most of the population is vaccinated, so the remaining infections are mild
• 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 influenza virus is too unstable to be cultured in the laboratory, so each new vaccine has to be grown in infected human volunteers
• CThe influenza virus hides its surface antigens beneath a lipid coat, so the immune system has nothing specific to recognise it by
• DThe immune system cannot form memory cells against viral antigens, only against bacteria, and so each infection produces a primary response

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 in the blood that carry out phagocytosis, so no pathogen can be engulfed and destroyed once they are lost
• BT helper cells are themselves the cells that secrete antibody directly into the plasma, so antibody production stops as their numbers fall
• 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 barrier (the skin) that blocks 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, each with its own specificity, and so one preparation recognises several epitopes
• BThey bind to any antigen they encounter without regard to its shape, which is why one preparation works against several pathogens
• 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, so just the variable binding sites remain and the immune system treats them as self

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.

What is an antigen?

• AA molecule that destroys an invading pathogen
• BA protein produced by a B lymphocyte cell
• CA molecule that triggers an immune response✓
• DA cell that engulfs and digests a pathogen

Answer: Antigens are usually surface proteins recognised as foreign, prompting the response. Antibodies are the proteins produced against them, and phagocytes are the cells that engulf.

What happens during phagocytosis?

• AThe pathogen is engulfed and digested by antibody molecules
• BThe pathogen is engulfed and digested by lysosomal enzymes✓
• CThe pathogen is bound by antibodies and left in the plasma
• DThe pathogen is destroyed by memory cells in the lymph node

Answer: A phagocyte engulfs the pathogen into a phagosome, which fuses with lysosomes so hydrolytic enzymes destroy it. The phagocyte then displays the antigens on its surface, linking innate and specific immunity.

What is the role of a helper T cell?

• ADestroying infected body cells by releasing perforin
• BProducing large quantities of specific antibody
• CEngulfing pathogens present in the bloodstream
• DStimulating B cells and cytotoxic T cells to respond✓

Answer: Helper T cells bind presented antigen and release cytokines that activate B cells, cytotoxic T cells and phagocytes. HIV destroys them, which is why the whole specific response collapses in AIDS. Perforin release is the cytotoxic T cell's job.

What is a plasma cell derived from, and what does it do?

• AA B cell, and it stores antigen for future recognition
• BA T cell, and it secretes large amounts of antibody
• CA T cell, and it engulfs pathogens by phagocytosis
• DA B cell, and it secretes large amounts of antibody✓

Answer: Clonal selection and expansion turn an activated B cell into plasma cells that pour out antibody, and into memory cells that persist. Plasma cells are short-lived — the memory cells give lasting immunity.

Why is the secondary immune response faster than the primary?

• AMemory cells are already present and secrete antibody
• BAntibodies from the first exposure remain in the blood
• CThe pathogen has mutated to a less harmful form
• DMemory cells are already present and divide rapidly✓

Answer: Memory B and T cells persist after the first exposure, so on re-exposure clonal expansion is much quicker and antibody concentration rises higher and sooner — usually before symptoms appear. Memory cells divide; plasma cells secrete.

What is the structure of an antibody?

• ATwo polypeptide chains with two variable binding regions
• BFour polypeptide chains with a single binding region
• COne polypeptide chain with four variable binding regions
• DFour polypeptide chains with two variable binding regions✓

Answer: Two heavy and two light chains form a Y shape, with variable regions at the tips of the arms giving specificity for one antigen. The constant region is the same across antibodies of a class.

Why does antigenic variability make vaccination difficult?

• AMemory cells become unable to divide after the change
• BThe pathogen becomes resistant to all known antibiotics
• CThe vaccine causes the pathogen to mutate more rapidly
• DMemory cells no longer recognise the changed antigens✓

Answer: If surface antigens change, existing memory cells no longer have complementary receptors and the response starts from scratch. That is why influenza vaccines are reformulated annually. Antibiotic resistance is a separate problem affecting bacteria.

What is herd immunity?

• AEvery member of a population has been successfully vaccinated
• BEnough of a population is immune that transmission is limited✓
• CA population develops immunity without any exposure at all
• DImmunity is passed from mother to offspring in breast milk

Answer: Once a high enough proportion is immune, an infected person is unlikely to meet a susceptible one, so chains of transmission break. It protects those who cannot be vaccinated, which is precisely why coverage thresholds matter.

What is passive immunity?

• AAntibodies are produced in response to a live vaccine
• BAntibodies are received ready-made from another source✓
• CMemory cells are produced following natural infection
• DMemory cells are received ready-made from another source

Answer: Passive immunity — across the placenta, in breast milk or by injection — gives instant protection but no memory cells, so it fades as the antibodies break down. Active immunity involves your own response and lasts far longer.