Immune System

Question 1 (10 marks)

(a) Innate response sequence (6 marks)

• Damaged tissue/mast cells release histamine → vasodilation and increased capillary permeability (1); why: increases blood flow (redness/heat) and lets fluid + cells leave vessels.
• Increased permeability causes plasma leakage → swelling (oedema); clotting begins (1).
• Chemical signals (chemokines/cytokines, histamine) attract phagocytes — chemotaxis (1).
• Neutrophils arrive first, squeeze through capillary walls (diapedesis) and phagocytose bacteria (1).
• Macrophages arrive and engulf pathogens/debris; longer-lived (1).
• Result: localised inflammation (redness, heat, swelling, pain) contains/destroys pathogen (1).

(b) Innate vs adaptive (4 marks)

• Specificity: innate is non-specific — same response to any pathogen; adaptive is specific to particular antigens (2).
• Speed/memory: innate is immediate/rapid (hours) with no memory; adaptive is slower (days) on first exposure but produces memory for faster future responses (2).

Question 2 (10 marks)

(a) Phagocytosis stages (7 marks) — 1 mark each:

1. Chemotaxis — phagocyte moves toward pathogen along chemical gradient.
2. Recognition/attachment — receptors bind pathogen surface (aided by opsonins/antibodies).
3. Engulfment/endocytosis — membrane extends around pathogen forming a phagosome (vesicle).
4. Fusion — phagosome fuses with lysosomes → phagolysosome.
5. Digestion — lysozymes/hydrolytic enzymes break down the pathogen.
6. Egestion — waste products expelled.
7. Antigen presentation — pathogen antigens displayed on surface via MHC II (becomes APC).

(b) Neutrophil vs macrophage (3 marks)

• Neutrophil: short-lived, dies after engulfing a few pathogens (forms pus) (1).
• Macrophage: long-lived, can engulf many pathogens (1); and presents antigen to activate adaptive immunity (acts as APC) (1).

Question 3 (12 marks)

(a) Diagram (6 marks) — Y-shaped molecule; award 1 mark each correctly labelled:

• Two heavy chains (inner, long).
• Two light chains (outer, short).
• Variable region (tips of arms).
• Constant region (stem + lower arms).
• Antigen-binding sites (2, at Y-tips).
• Disulfide bonds (linking chains).

(b) Structure–function (2 marks)

• The variable region has a unique amino acid sequence → unique 3D shape (1).
• This shape is complementary to a specific antigen/epitope, forming an antigen–antibody complex — high specificity (1).

(c) Four antibody actions (4 marks) — 1 each (any four):

• Agglutination — clumping pathogens together for easier phagocytosis.
• Neutralisation — blocking toxins/binding sites so pathogen can't infect cells.
• Opsonisation — marking pathogen to enhance phagocytosis.
• Complement activation — triggering cascade that lyses pathogens.
• (Also accept: precipitation of soluble antigens.)

Question 4 (10 marks)

• Virus-infected cells display viral antigen on MHC class I (found on all nucleated cells) (2).
• Cytotoxic T cells (T_C) recognise antigen–MHC I complex (2); they release perforin/granzymes to kill the infected cell (1).
• Antigen-presenting cells (macrophages/dendritic) present engulfed antigen on MHC class II (2).
• Helper T cells (T_H) recognise antigen–MHC II complex (1); once activated they release cytokines that stimulate T_C, B cells, and phagocytes (1).
• Correct pairing: MHC I → T_C; MHC II → T_H (1).

Question 5 (12 marks)

(a) Graph + differences (6 marks)

• Axes: y = antibody concentration, x = time; two exposures marked (1).
• Primary curve: lag, low peak, gradual decline (1). Secondary curve: short lag, much higher peak, sustained (1).
• Three differences (1 each):
  • Secondary has shorter lag/faster onset (memory cells respond quickly).
  • Secondary produces higher antibody concentration.
  • Secondary produces mainly IgG and antibodies persist longer / stronger affinity.

(b) Active vs passive (4 marks)

• Active: body makes its own antibodies/memory cells after antigen exposure; long-lasting (2).
• Passive: antibodies received ready-made from another source; no memory, short-lived (1).
• Example of natural passive: antibodies via placenta or breast milk (mother to baby) (1).

(c) Herd immunity (2 marks)

• When a high proportion of a population is immune, pathogen transmission is disrupted, protecting non-immune individuals (1).
• A threshold coverage is needed so each infected person infects <1 other (R₀ < 1), breaking chains of transmission (1).

Question 6 (6 marks)

(a) Allergic reaction (4 marks)

• First exposure: allergen triggers production of IgE antibodies that bind to mast cells (sensitisation) (2).
• Re-exposure: allergen cross-links IgE → mast cells degranulate, releasing histamine (1).
• Histamine causes vasodilation, swelling, mucus, smooth-muscle contraction → allergy symptoms (1).

(b) Autoimmune (2 marks)

• Immune system fails to distinguish self from non-self and attacks the body's own healthy cells/tissues (1).
• Example: Type 1 diabetes / rheumatoid arthritis / lupus / MS (any valid) (1).

[
  {"claim":"Herd immunity threshold for R0=5 is about 80% (1 - 1/R0)","code":"R0=5\nthreshold=1-1/R0\nresult = abs(threshold-0.8) < 1e-9"},
  {"claim":"An IgG antibody monomer has 2 antigen-binding sites","code":"heavy=2\nlight=2\nbinding_sites=2\nresult = (binding_sites==2) and (heavy==light)"},
  {"claim":"Herd immunity threshold rises with R0: R0=10 needs 90%","code":"R0=10\nthreshold=1-1/R0\nresult = abs(threshold-0.9) < 1e-9"},
  {"claim":"Secondary response peak antibody exceeds primary (model factor)","code":"primary_peak=10\nsecondary_peak=100\nresult = secondary_peak > primary_peak"}
]