Unit 13 Question Bank
The five tabs are the five sections of the real paper. Items tagged
Past Paper 2019 or 2020 are the genuine questions, reproduced verbatim.
Items tagged Slide come from the TMU lecture; items tagged Janeway's are built
from the textbook to cover examinable ground. Nothing is invented. Janeway's 10e is a reflowed
edition with no printed page numbers, so it is cited by numbered section (§1-14), not by page.
0 / 28 answered
1Which of the following cells is not involved in type I hypersensitivity?
Answer: A
Mast cells and basophils are the primary effectors, both bearing FcεRI; eosinophils join the late-phase reaction. The NK cell belongs to type II, where it performs ADCC via FcγRIII. The distinction: ADCC needs IgG on a target cell, whereas type I has IgE on a mast cell.Past Papers 2019 & 2020, Section III Q17 — verbatim, both years
2In the following diseases, which one is caused by type I hypersensitivity?
Answer: B
Allergic rhinitis (hay fever) is IgE-mediated type I. The distractors are one per type: serum sickness is type III, rheumatoid arthritis largely type III, haemolytic anaemia type II. The question is asking whether you can place four diseases in four boxes.Past Papers 2019 & 2020, Section III Q20 — verbatim, both years
3Which immunoglobulin mediates type I hypersensitivity?
Answer: C
IgE — the least abundant serum immunoglobulin, which does not fix complement, and which binds FcεRI on mast cells and basophils through its CH2 and CH3 domains.TMU Lecture 11 — Hypersensitivity Slide 35
4IgE binds to FcεRI through which domains?
Answer: D
The Fc region binds the receptor while the variable region stays free to catch allergen — which is exactly what allows a mast cell to sit pre-armed and waiting.TMU Lecture 11 — Hypersensitivity Slide 35
5An allergen is best defined as an antigen that:
Answer: A
Allergens are proteins — only proteins can be presented to T cells — that typically reach mucosal surfaces at very low doses. Th2 makes IL-4, IL-4 drives class switching to IgE, and IgE arms the mast cell.TMU Lecture 11 — Hypersensitivity Slide 29
6What triggers mast cell degranulation in type I hypersensitivity?
Answer: B
One allergen must bridge two IgE molecules, pulling two receptors together — which is why an allergen must be at least bivalent, and why desensitization with tiny repeated doses prevents the reaction.TMU Lecture 11 — Hypersensitivity Slide 43
7Which is the preformed mediator stored in mast cell granules?
Answer: C
Histamine is preformed and released immediately. Leukotrienes, PGD₂ and PAF are newly formed — synthesised after activation, so they act later and drive the late phase.TMU Lecture 11 — Hypersensitivity Slide 39
8The three tissue effects of type I mediators are:
Answer: D
Every symptom of every type I disease is one of these three happening somewhere particular — nose gives rhinitis, bronchi asthma, skin urticaria, gut vomiting, and everywhere at once anaphylaxis. The other options describe types II, III and IV respectively.TMU Lecture 11 — Hypersensitivity Slides 45, 47
9In the sensitization phase of type I hypersensitivity:
Answer: A
Sensitization is silent — the patient feels nothing. Cross-linking is the excitation phase on second exposure; mediator action is the effector phase. This is exactly what happened to Portier and Richet's dogs: the first injection was tolerated, the second killed them.TMU Lecture 11 — Hypersensitivity Slide 42
10Which cells express the high-affinity IgE receptor FcεRI?
Answer: B
Mast cells and basophils carry it at high density and are the primary effectors; eosinophils also express it, participate in the late-phase reaction, and additionally down-regulate the response through some of their mediators.TMU Lecture 11 — Hypersensitivity Slides 36–38
11A positive skin test for type I hypersensitivity is read as:
Answer: C
The 30-minute timing marks it as immediate. Red induration at 24–48 hours is the tuberculin test — type IV — and confusing the two timings confuses the two mechanisms.TMU Lecture 11 — Hypersensitivity Slide 55
12What is the main risk of skin testing?
Answer: D
Its advantages are that it is relatively inexpensive and screens many allergens at once; the disadvantage is that introducing allergen into a sensitized person can, rarely, trigger the very systemic reaction you were testing for.TMU Lecture 11 — Hypersensitivity Slide 56
13Desensitization differs from hyposensitization in that desensitization uses:
Answer: A
Short interval = desensitization: each tiny dose releases a little mediator, and repeating before the granules refill empties them — temporary protection, used to give antitoxin today. Long interval = hyposensitization: repeated exposure shifts antibody production from IgE to IgG, which then blocks allergen — slow but lasting.TMU Lecture 11 — Hypersensitivity Slide 59
14Systemic anaphylaxis causes a fall in blood pressure because of:
Answer: B
Mediators released everywhere at once cause fluid to leave the circulation throughout the body — a shock-like and often fatal state with onset within minutes. Widespread microthrombi belong to type III.TMU Lecture 11 — Hypersensitivity Slide 50
15Which Th subset drives type I hypersensitivity?
Answer: C
Th2 secretes IL-4, which drives B-cell class switching to IgE. Th1 drives type IV. This pairing is True/False Q11, and it is the Unit 5 Th1/Th2 table doing clinical work.Past Papers 2019 & 2020, Section IV Q11 · TMU Lecture 11 — Hypersensitivity Slide 29
16Which classification of hypersensitivity is used, and by whom?
Answer: D
Gell and Coombs classified hypersensitivity into four types by mechanism. Portier and Richet discovered anaphylaxis — Richet won the Nobel Prize in 1913 — but did not produce the classification.TMU Lecture 11 — Hypersensitivity Slide 21
1 Hypersensitivity — 3 marks+
When the immune system is re-exposed to the same antigen, the immune response is enhanced. Under some circumstances this enhanced response has deleterious effects, resulting in functional disorder, tissue damage or even death. This inappropriate or pathological immune response is termed hypersensitivity or allergy, and it is specific. Gell and Coombs classified it into four types by mechanism.Past Papers 2019 AND 2020, Section I · TMU Lecture 11 — Hypersensitivity Slides 20–21
2 Allergen — 3 marks+
An antigen that selectively activates CD4⁺ Th2 cells and B cells and induces an IgE antibody response. Allergens are proteins — only proteins can be presented to T cells — and generally reach mucosal surfaces at very low doses: pollens, dust mites, spores, animal dander, foods.TMU Lecture 11 — Hypersensitivity Slide 29
3 Type I hypersensitivity — 3 marks+
Anaphylactic or immediate hypersensitivity, mediated by IgE. Components: allergen · IgE · mast cells and basophils (with eosinophils in the late phase) · mediators. Three phases: sensitization (IgE binds FcεRI), excitation (allergen cross-links FcεR → degranulation) and effector (mediators act). Diseases: asthma, allergic rhinitis, urticaria, anaphylaxis.TMU Lecture 11 — Hypersensitivity Slides 22, 41–46
4 Mediators of type I hypersensitivity — 3 marks+
Preformed — made before degranulation and stored in granules: histamine. Newly formed — synthesised after activation: leukotrienes (LTs), prostaglandin D₂ and PAF. All produce three tissue effects: smooth-muscle contraction, vasodilation with increased vascular permeability, and mucus secretion.TMU Lecture 11 — Hypersensitivity Slides 39, 45
5 Desensitization and hyposensitization — 3 marks+
Desensitization — repeated injection of small amounts of allergen at short intervals (20–30 min), which gradually exhausts the active mediators; used to give antitoxin to a sensitized patient. Hyposensitization — repeated small doses at long intervals (5–7 days), which shifts antibody production from IgE to IgG.TMU Lecture 11 — Hypersensitivity Slide 59
1The four components of type I hypersensitivity are ? , the antibody ? , the cells ? and ? , and the ? .5 mark(s)
Eosinophils join in the late-phase reaction and also down-regulate the response.
TMU Lecture 11 — Hypersensitivity Slide 282The three phases of type I hypersensitivity are the ? phase, the ? phase and the ? phase.3 mark(s)
Sensitization is silent; the second exposure causes the reaction.
TMU Lecture 11 — Hypersensitivity Slide 413IgE binds ? on mast cells and basophils through its ? and ? domains.3 mark(s)
The Fc binds the receptor while the variable region stays free to catch allergen.
TMU Lecture 11 — Hypersensitivity Slide 354The preformed mediator is ? ; three newly formed mediators are ? , ? and ? .4 mark(s)
Preformed acts immediately; newly formed drive the late phase.
TMU Lecture 11 — Hypersensitivity Slide 395Mediators of type I cause ? contraction, ? with increased vascular ? , and ? secretion.4 mark(s)
Three effects; the site of the mast cells decides which disease results.
TMU Lecture 11 — Hypersensitivity Slide 476A positive skin test shows a ? and ? greater than 5 × 5 mm after ? minutes.3 mark(s)
Thirty minutes marks it as immediate — contrast the tuberculin test at 24–48 hours.
TMU Lecture 11 — Hypersensitivity Slide 551IgE fixes complement.
FALSE
False. IgE does not fix complement — one of its listed properties. Its mechanism is entirely FcεRI-mediated mast-cell degranulation, which is also why complement plays no part in type I.TMU Lecture 11 — Hypersensitivity Slide 35
2The first exposure to an allergen causes the clinical symptoms of type I hypersensitivity.
FALSE
False. The first exposure sensitizes — IgE is made and binds FcεRI, silently. It is the second exposure that cross-links and causes degranulation.TMU Lecture 11 — Hypersensitivity Slides 42–43
3Th2 cells are involved in type I hypersensitivity.
TRUE
True — half of True/False Q11. Th2 secretes IL-4, which drives B-cell class switching to IgE. The other half, Th1 driving type IV, is also true.Past Papers 2019 & 2020, Section IV Q11
4A single IgE molecule binding a single allergen is sufficient to trigger degranulation.
FALSE
False. One allergen must bridge two adjacent IgE molecules to cross-link the receptors — which is why an allergen must be at least bivalent, and why desensitization works.TMU Lecture 11 — Hypersensitivity Slide 43
5Eosinophils only amplify type I hypersensitivity and never limit it.
FALSE
False. Eosinophils participate in the late-phase reaction and down-regulate type I hypersensitivity through some of the mediators they synthesise and release.TMU Lecture 11 — Hypersensitivity Slide 38
6Hyposensitization works by shifting antibody production from IgE to IgG.
TRUE
True. Long intervals (5–7 days) of small allergen doses shift the B-cell response toward IgG, which then blocks allergen before it reaches mast-cell IgE. Desensitization, at 20–30 minute intervals, works differently — by exhausting the mediators.TMU Lecture 11 — Hypersensitivity Slide 59
1
Describe the mechanism of type I hypersensitivity.
6 marks
Components. ① Allergens — proteins that selectively activate Th2 and B cells to induce IgE. ② IgE — least abundant serum Ig, does not fix complement, binds FcεRI via CH2 and CH3. ③ Cells — mast cells and basophils (both FcεRI⁺), with eosinophils in the late phase. ④ Mediators.
① Sensitization phase. First allergen exposure activates B cells to form IgE-secreting plasma cells; IgE binds FcεRI on mast cells and basophils, producing sensitized target cells. No symptoms.
② Excitation phase. The allergen re-enters and cross-links the bound IgE, changing the target-cell membrane and triggering degranulation.
③ Effector phase. Preformed histamine and newly formed leukotrienes, PGD₂ and PAF cause smooth-muscle contraction, vasodilation with increased vascular permeability, and mucus secretion — giving rhinitis, asthma, urticaria or anaphylaxis according to site.
Marking guide: 2 marks per phase, or 1.5 per phase plus 1.5 for the components. The cross-linking step is the mechanistic core and must be explicit.
2
How is type I hypersensitivity detected and treated?
6 marks
Detection. ① Skin test — small amounts of allergen by intradermal injection or superficial scratching of forearm skin; a wheal and flare >5 × 5 mm at 30 minutes is positive, showing specific IgE on skin mast cells. Advantages: inexpensive, screens many allergens at once. Disadvantage: rarely may induce systemic anaphylactic shock. ② ELISA for serum IgE specific to a given allergen.
Treatment principles. ① Avoid known allergens. ② Inhibit IgE production. ③ Stabilise mast cells to inhibit degranulation. ④ Antagonise active mediators. ⑤ Medication, including:
| Desensitization | Hyposensitization | |
|---|---|---|
| Method | Small doses, short intervals (20–30 min) | Small doses, long intervals (5–7 days) |
| Mechanism | Gradually exhausts the active mediators | Shifts antibody production from IgE to IgG |
Marking guide: 2 marks for detection, 2 for the five principles, 2 for the desensitization/hyposensitization contrast — interval and mechanism must both be right.
3
List the common diseases caused by type I hypersensitivity.
6 marks
Systemic anaphylaxis — a shock-like, often fatal state with onset within minutes, caused by systemic vasodilation and increased permeability. Causes: drugs (penicillin, insulin), animal antiserum antitoxins, and venom from bee, wasp or hornet.
Respiratory. Allergic rhinitis (hay fever) — airborne allergens meet sensitized mast cells in conjunctivae and nasal mucosa; watery exudation, sneezing, coughing. Asthma — the same reaction in the lower respiratory tract; bronchial smooth-muscle contraction and mucus secretion cause airway obstruction and dyspnoea.
Skin. Atopic urticaria (hives) — allergen binds sensitized mast cells in skin, causing swollen red eruptions; also eczema.
Digestive. IgE cross-linking on GI mast cells causes localised smooth-muscle contraction and vasodilation — vomiting, diarrhoea, bellyache.
All share one mechanism; the site of the degranulating mast cells determines the disease. 20–30% of the population is affected by some form.
Marking guide: 1.5 marks per system. Stating that a single mechanism produces different diseases according to site is what lifts a list into an answer.