Covers Lessons 08–13: plant and animal responses to pathogens, innate immunity, adaptive immunity (humoral and cell-mediated), and primary vs secondary immune response.
Plant responses to pathogens — physical, chemical, hypersensitive response, Banksia
Animal physical/chemical responses — inflammation, fever, chemical mediators
Innate immune system — phagocytosis, NK cells, complement, interferons
Antigens, antibodies, clonal selection, humoral immunity, memory B cells
T cells, cell-mediated immunity, MHC classes, T helper coordination
Primary/secondary response, vaccination, Jenner, herd immunity, passive immunity
The hypersensitive response (HR) in plants is best described as:
Salicylic acid (SA) produced at a localised Phytophthora infection site in a Banksia root travels to uninfected shoots. This represents:
The swelling observed at a site of bacterial infection is caused primarily by:
Ibuprofen reduces fever and pain by inhibiting the enzyme COX (cyclooxygenase). This works because COX is required for the synthesis of:
Interferons are released by virus-infected cells. Their primary function is to:
Natural killer (NK) cells detect virus-infected host cells by:
During phagocytosis, the phagolysosome is formed when:
Dendritic cells are described as bridging innate and adaptive immunity because they:
The variable region of an antibody molecule determines:
Clonal selection refers to the process by which:
An antibody binds to a bacterial surface protein, making the bacterium significantly easier for neutrophils to engulf. This mechanism is called:
MHC class I molecules differ from MHC class II molecules in that MHC class I:
When a cytotoxic T cell kills a virus-infected host cell, the mechanism involves:
HIV progressively destroys CD4+ T helper cells. The most significant immunological consequence is that:
The secondary immune response produces antibody levels 10–100 times higher than the primary response primarily because:
Edward Jenner's cowpox vaccination protected against smallpox because:
Passive immunity differs from active immunity in that passive immunity:
The hypersensitive response (HR) in plants and cytotoxic T cell killing in animals are both strategies for limiting pathogen spread. Which statement correctly compares these two mechanisms?
A patient with a genetic deficiency that prevents complement protein production would most likely experience difficulty with which combination of immune functions?
A person receives their first influenza vaccine. Two weeks later they experience mild fatigue and a low-grade fever. A year later, after receiving their annual influenza booster, they feel nothing. Which explanation best accounts for this difference?
Multiple Choice Result
Compare the innate and adaptive immune systems across four features: speed, specificity, memory, and the key cells involved. Explain why both systems are necessary for effective defence against pathogens. (4 marks)
1 mark per correctly compared feature (speed, specificity, memory, key cells) | 1 mark: explanation of why both are necessary (innate provides immediate containment; adaptive provides targeted elimination and memory)
Speed: The innate immune system responds within minutes to hours of pathogen detection — always ready, pre-formed. The adaptive immune system requires 7–14 days to reach peak effectiveness as naive B and T cells must undergo clonal selection, clonal expansion, and differentiation.
Specificity: The innate system is non-specific — it uses pattern recognition receptors (PRRs) to detect broad molecular patterns (PAMPs) shared by many pathogens (e.g. LPS, viral RNA). The adaptive system is highly specific — each B or T cell has a unique receptor for one specific antigen.
Memory: Classical innate immunity has no memory — the same response occurs every time. The adaptive system generates immunological memory (memory B and T cells) that enables a faster, stronger secondary response on re-exposure.
Key cells: Innate: neutrophils, macrophages, dendritic cells, NK cells, mast cells. Adaptive: B lymphocytes (→ plasma cells and memory B cells), T helper cells (CD4+), cytotoxic T cells (CD8+).
Why both are necessary: The innate system is essential for immediate containment — without it, pathogens would replicate unchecked during the days it takes the adaptive system to respond. The adaptive system is essential for targeted pathogen elimination, clearing intracellular infections (via CTLs) that the innate system cannot resolve, and forming lasting memory. The innate system also activates and shapes the adaptive response — dendritic cells bridge the two systems.
Describe the sequence of events from antigen entry to antibody production in humoral immunity. Then explain the role of T helper cells in this process and what would happen if T helper cells were absent. (4 marks)
1 mark: antigen presentation by dendritic cell on MHC II | 1 mark: clonal selection of matching B cell + T helper co-stimulation | 1 mark: clonal expansion → plasma cells + memory B cells | 1 mark: consequence of T helper absence — inadequate B cell activation, no class switching, impaired memory
When an antigen enters the body, dendritic cells (and macrophages) engulf it, process it, and present antigen fragments on MHC class II molecules. These antigen-presenting cells migrate to lymph nodes where naive B cells circulate. Through clonal selection, the rare B cell whose B cell receptor (BCR) matches the specific antigen binds it. However, this alone is insufficient for full activation — the B cell also requires a co-stimulatory signal from a T helper cell (CD4+) that has independently recognised the same antigen on MHC class II. This dual signal prevents accidental B cell activation against self-antigens. Once activated, the B cell undergoes clonal expansion — rapidly dividing to produce a large clone. These differentiate into plasma cells (short-lived antibody factories secreting thousands of specific antibodies per second) and memory B cells (long-lived, persist for years).
If T helper cells were absent (as in late-stage HIV infection), B cells cannot receive the co-stimulatory signal required for full activation and antibody class switching. They may produce some IgM (T-independent antigens can trigger limited responses) but cannot generate high-affinity IgG or form effective memory. Both arms of adaptive immunity are compromised simultaneously.
A previously unvaccinated adult is exposed to tetanus bacteria through a deep wound. They are treated with tetanus immunoglobulin (pre-formed antibodies) and then given their first tetanus toxoid vaccine. Ten years later they receive a tetanus booster. Using your knowledge of passive and active immunity, primary and secondary immune responses, and memory cells, explain: (i) why the immunoglobulin was given immediately; (ii) what the vaccine did; and (iii) why a booster was needed ten years later. (4 marks)
1 mark: immunoglobulin = passive immunity — immediate protection while adaptive response develops | 1 mark: vaccine = active immunisation — primary response → memory cells | 1 mark: booster = secondary response via memory cells — faster, higher | 1 mark: booster needed because memory cell numbers and antibody levels decline over time without re-exposure
(i) Immunoglobulin — immediate passive immunity: Tetanus toxin acts rapidly and can cause life-threatening illness before the adaptive immune system has time to respond. The adult has no prior immunity (no memory cells, no circulating antibodies). Tetanus immunoglobulin provides passive immunity — pre-formed antibodies that immediately neutralise tetanus toxin. This is temporary (the antibodies are gradually catabolised over weeks) but provides protection during the critical period. No memory cells are formed — passive immunity does not trigger clonal selection.
(ii) Vaccine — active immunisation, primary response: The tetanus toxoid vaccine introduces inactivated tetanus toxin (toxoid) — an antigen that cannot cause disease. The immune system mounts a primary response: dendritic cells present tetanus antigens, the matching B cell clone undergoes clonal selection (with T helper co-stimulation), and clonal expansion produces plasma cells (generating tetanus-specific antibodies) and memory B and T cells. These memory cells persist long-term. The vaccine takes 1–2 weeks to provide effective active immunity — which is why the immunoglobulin was needed in the interim.
(iii) Booster — secondary response, reinforce fading memory: Memory B and T cell populations are not permanent — without re-exposure or booster doses, their numbers decline gradually over years, and antibody levels fall below the protective threshold. Ten years after the primary vaccine, protection may have waned. The booster dose re-exposes the immune system to tetanus toxoid, triggering a secondary response: memory B cells rapidly activate and differentiate into plasma cells within 1–3 days, producing high-affinity IgG at much higher levels than the original primary response. The booster both restores protective antibody levels immediately and expands the memory cell population — resetting the clock on protection for another decade.