Biology • Year 12 • Module 7 • Lesson 10
The Innate Immune System
Build HSC Band 5–6 extended-response technique — evaluate innate immunity using sea urchin comparative data and assess a viral immunology claim.
1. Data + scenario — the sea urchin as a model of innate-only immunity (Band 5–6)
8 marks Band 5–6
Stimulus. The purple sea urchin (Strongylocentrotus purpuratus) is a well-studied model for innate immunity. Unlike vertebrates, sea urchins have no adaptive immune system — no B cells, no T cells, no antibodies, no immunological memory of the classical kind. Yet S. purpuratus can live for over 100 years in shallow marine environments teeming with bacteria and viruses. Their genome encodes more than 200 different pattern recognition receptor (PRR) genes, compared to roughly 10 functional PRR variants in the average human. The table below shows immune response measurements from a study in which sea urchins were injected with Vibrio diazotrophicus (a gram-negative bacterium) and compared to control (saline-injected) animals over 72 hours (after Matranga et al. 2006, Cell Stress and Chaperones).
| Measurement | Control (0 h) | 4 h post-injection | 24 h post-injection | 72 h post-injection |
|---|---|---|---|---|
| Coelomocyte (immune cell) count (cells/mL) | 1.2 × 10⁶ | 3.8 × 10⁶ | 6.1 × 10⁶ | 4.0 × 10⁶ |
| Phagocytic activity index (%) | 22 | 61 | 78 | 55 |
| Clotting response (scale 0–3) | 0.1 | 1.8 | 2.4 | 1.2 |
| Bacterial load in coelomic fluid (CFU/mL × 10³) | 0 | 420 | 85 | 8 |
Q1. Analyse and evaluate, using the stimulus data and your lesson content, how effectively the sea urchin's innate immune system responds to bacterial infection. In your response you must:
- Identify the trend in at least two measurements from the data table and link each trend to a named innate immune mechanism.
- Compare the sea urchin's immune response to the vertebrate innate immune response, identifying one similarity and one key difference.
- Evaluate what the bacterial load data suggests about the overall effectiveness of innate-only immunity in this model organism.
- Assess whether the lesson's claim that "innate immunity can contain infections entirely on its own" is supported by these data, and reach an evidence-based judgement.
2. Source critique — evaluate a textbook claim (Band 5–6)
7 marks Band 5–6
"The innate immune system and the adaptive immune system operate completely independently. The innate system provides a short, non-specific attack before switching off as soon as the adaptive system takes over. Natural killer cells are part of the adaptive system because they kill pathogens directly, and their activity requires prior sensitisation to a specific pathogen antigen. The innate system produces no useful information for the adaptive system — antibodies are the first step in any coordinated immune response."
— Source: fictional Year 12 biology revision guide, 2022.
Q2. Evaluate the claim above. Identify each specific error the passage makes, explain the correct biology for each, and conclude with a biologically accurate summary statement about the relationship between the innate and adaptive immune systems and the role of NK cells.
Q1 — Sample Band 6 response (8 marks), annotated
The data show a co-ordinated, multi-phase innate immune response. [orientation]
Coelomocyte count rises from 1.2 × 10⁶ cells/mL at 0 hours to a peak of 6.1 × 10⁶ cells/mL at 24 hours — a five-fold increase — before declining to 4.0 × 10⁶ at 72 hours. This mirrors the vertebrate innate response in which phagocytes (neutrophils in vertebrates, coelomocytes in sea urchins) are rapidly recruited to an infection site via chemokine-driven chemotaxis and diapedesis. The rise reflects recruitment and the decline reflects cell death after pathogen clearance. [1 — first trend + named mechanism]
Phagocytic activity index follows a similar pattern, rising from 22% to a peak of 78% at 24 hours then partially resolving. This directly parallels the phagocytosis mechanism described in the lesson — the increase in phagocytic activity indicates that coelomocytes are engulfing Vibrio bacteria, forming phagosomes, fusing lysosomes to form phagolysosomes, and destroying the bacteria with digestive enzymes. [1 — second trend + mechanism]
Crucially, bacterial load data show the innate response is effective: starting from 420 × 10³ CFU/mL at 4 hours, bacterial load falls to 85 × 10³ at 24 hours and to just 8 × 10³ at 72 hours — a 98% reduction achieved entirely through innate mechanisms. [1 — bacterial load analysed]
Comparing to vertebrate innate immunity: the similarity is the use of non-specific PRR-based detection of PAMPs on gram-negative bacteria (e.g. LPS detection), and the subsequent phagocytic response. The key difference is that vertebrates have only approximately 10 functional PRR variants (plus a full adaptive immune system), while S. purpuratus encodes over 200 PRR genes — a compensation for having no B or T cells. Sea urchins cannot produce antibodies, cannot form memory lymphocytes, and cannot mount a clonally expanded adaptive response. [1 — similarity; 1 — difference]
The bacterial load data strongly support the lesson's claim that innate immunity can contain infections entirely on its own. Despite having no adaptive immune system at all, the sea urchin eliminates 98% of an injected bacterial load within 72 hours through phagocytosis, clotting and other innate mechanisms alone. [1 — evaluates claim with data]
My evidence-based judgement is that innate-only immunity is sufficient for infections by pathogens that lack evasion strategies specifically tailored to circumvent PRRs or phagocytosis. The lesson notes that humans with innate deficiencies die from infections others never notice; the sea urchin data show the inverse — that even without adaptive immunity, a sufficiently broad PRR repertoire and active phagocytic system can successfully clear common bacterial pathogens. The limitation is evolution: pathogens can evolve to evade PRR detection, and without adaptive specificity and memory, a sea urchin re-exposed to a pathogen that has mutated would have the same PRR-based response — no memory advantage. [1 — evidence-based judgement acknowledging limits]
Marking criteria.
- 1 mark — Identifies trend in coelomocyte count (rises then falls) and links to phagocyte recruitment via chemotaxis / equivalent mechanism.
- 1 mark — Identifies trend in phagocytic activity index and links to phagocytosis steps (phagosome → phagolysosome → enzymatic digestion).
- 1 mark — Analyses bacterial load data with specific values — identifies 98% reduction and links to innate mechanisms.
- 1 mark — Identifies one similarity between sea urchin and vertebrate innate immunity (PRR/PAMP-based non-specific detection; phagocytic response).
- 1 mark — Identifies one key difference (no adaptive system; broader PRR repertoire; no antibodies/memory cells; coelomocytes vs neutrophils/macrophages).
- 1 mark — Evaluates the lesson's claim using the data — argues for or against "innate alone can contain infection" with data-based reasoning.
- 1 mark — Reaches an explicit, evidence-based judgement that goes beyond the data to address conditions under which innate-only immunity is or is not sufficient.
- 1 mark — Response uses precise lesson terminology throughout (PAMPs, PRRs, phagocytosis, chemotaxis, innate, adaptive) and maintains a coherent logical structure from data → mechanism → comparison → judgement.
Q2 — Sample Band 6 response (7 marks)
The passage contains six identifiable biological errors. [1 — overall evaluative framing]
Error 1 — "completely independent." Incorrect. The innate and adaptive systems are tightly integrated. Dendritic cells, for example, are innate cells that engulf and process antigens (innate function) and then migrate to lymph nodes to present antigen fragments on MHC II to naive T cells — directly initiating the adaptive response. The cytokine environment created by innate cells also determines what type of adaptive response is mounted. [1 — refutes "independent" with dendritic cell bridge]
Error 2 — "switching off as soon as adaptive takes over." Incorrect. Both systems operate simultaneously during an active infection. Innate mechanisms (phagocytosis by macrophages, complement activity, NK cell killing) continue throughout the adaptive response and are enhanced by adaptive products such as antibodies (which opsonise pathogens for phagocytosis). [1 — refutes "switch off"]
Error 3 — "NK cells are part of the adaptive system." Incorrect. NK cells are innate lymphocytes. They require no prior sensitisation, do not undergo clonal expansion, and mount the same response regardless of previous exposure. They are classified within the innate immune system. [1 — refutes NK cell classification]
Error 4 — "kill pathogens directly." Incorrect. NK cells do not engulf pathogens — that is the function of phagocytes (neutrophils and macrophages). NK cells kill infected host cells by releasing perforin (pore-forming protein) and granzymes (pro-apoptotic enzymes). They target cells with reduced MHC class I — a "missing self" strategy. [1 — refutes "kill pathogens directly"]
Error 5 — "prior sensitisation required." Incorrect. NK cells are always ready — one of the defining features of innate immunity is that it requires no prior sensitisation. It is cytotoxic T cells (adaptive) that require antigen presentation, clonal expansion and several days to reach full activity. [included in mark 3 or 4]
Error 6 — "antibodies are the first step." Incorrect. Antibodies are produced by B lymphocytes of the adaptive immune system, which takes days to weeks to activate and requires antigen presentation from the innate system to get started. The first step in a coordinated immune response is innate — mast cell degranulation, complement activation, and phagocyte recruitment occur within minutes to hours before any antibodies are produced. [1 — refutes "antibodies first"]
Accurate summary statement: The innate and adaptive immune systems are co-ordinated and interdependent. The innate system responds first (within minutes), contains many infections entirely, activates the adaptive system via antigen-presenting cells such as dendritic cells, and continues to operate throughout the adaptive response. NK cells are innate lymphocytes that kill virus-infected host cells using a non-specific "missing self" strategy — they do not require prior sensitisation and do not target pathogens directly. Antibodies are a product of adaptive immunity and cannot be produced before the adaptive system is activated by innate signals. [1 — accurate summary integrating all corrections]
Marking criteria.
- 1 mark — States an overall evaluative judgement (e.g. "the passage contains multiple significant errors").
- 1 mark — Correctly refutes "completely independent" — identifies dendritic cells (or cytokines/complement) as a bridge between innate and adaptive systems.
- 1 mark — Correctly refutes "switch off" — explains that both systems operate simultaneously during an active infection.
- 1 mark — Correctly classifies NK cells as innate lymphocytes — explains no prior sensitisation is required and contrasts with cytotoxic T cells.
- 1 mark — Correctly refutes "kill pathogens directly" — explains that NK cells kill infected host cells (not pathogens) using perforin/granzymes and the "missing self"/MHC I strategy.
- 1 mark — Correctly refutes "antibodies are the first step" — explains that antibodies are produced by the adaptive system, which is activated by innate signals; innate responses (complement, mast cells, phagocytes) occur first.
- 1 mark — Provides a coherent accurate summary statement integrating the corrected biology: innate and adaptive are interdependent; NK cells are innate; antibodies are adaptive; innate responds first and activates adaptive.