Unit 15 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
1In the following diseases, which one is caused by type III hypersensitivity?
Answer: C
SLE is the archetypal immune-complex disease, driven by antinuclear antibodies against DNA and histones. The distractors are one per type: asthma is type I; tuberculosis and contact dermatitis are both type IV.Past Papers 2019 & 2020, Section III Q18 — verbatim, both years
2Which size of immune complex causes immune-complex disease?
Answer: D
A Goldilocks problem. Large complexes are cleared rapidly by phagocytes; small ones are filtered by the glomerulus and do not activate complement. Medium complexes are too small to be phagocytosed and too large to filter — so they deposit, and they activate complement strongly.TMU Type III & IV Hypersensitivity deck Slide 4
3Where do immune complexes characteristically deposit?
Answer: A
All three are sites where blood is filtered under pressure through small vessels — which is why the clinical picture of immune-complex disease is arthritis, nephritis and occasionally cerebral involvement.TMU Type III & IV Hypersensitivity deck Slide 3
4Which cell causes most of the tissue damage in type III hypersensitivity?
Answer: B
Complement fragments C3a, C5a and C5b67 are chemotactic and recruit neutrophils, which release lytic enzymes. The antibody itself does almost none of the damage — it deposits, complement amplifies, and neutrophils destroy.TMU Type III & IV Hypersensitivity deck Slides 6, 8
5Which complement fragments recruit neutrophils in type III hypersensitivity?
Answer: C
These are the chemotactic factors. The same C3a and C5a also act as anaphylatoxins, degranulating mast cells and increasing vascular permeability; C3b separately activates platelets, which aggregate into microthrombi.TMU Type III & IV Hypersensitivity deck Slide 6
6Serum sickness typically appears how long after antiserum is given?
Answer: D
Type III must wait for a primary antibody response to occur before complexes can form — hence 1–2 weeks. The timings are diagnostic: type I is minutes, type IV is 24–72 hours, type III is 1–3 weeks.TMU Type III & IV Hypersensitivity deck Slide 11
7Rheumatoid factor is:
Answer: A
The auto-antigen is degenerated IgG and the auto-antibody is anti-IgG — rheumatoid factor, an IgM. The resulting complexes deposit in the synovium of small joints, giving symmetrical, progressive, destructive lesions and eventual deformity.TMU Type III & IV Hypersensitivity deck Slide 14
8The auto-antibody characteristic of SLE is:
Answer: B
ANA is directed against DNA and histones. Symptoms are fever, weakness, arthritis, skin rashes and kidney dysfunction — the distribution you would predict from where immune complexes deposit.TMU Type III & IV Hypersensitivity deck Slide 17
9Post-streptococcal glomerulonephritis appears how long after infection?
Answer: C
Anti-streptococcal antibody meets soluble streptococcal antigen, forming circulating complexes that deposit on the glomerular basement membrane. Note this is a different mechanism from rheumatic fever, which is type II cross-reaction.TMU Type III & IV Hypersensitivity deck Slide 13
10Farmer's lung and pigeon breeder's lung are examples of:
Answer: D
Immune complexes deposit on the alveolar wall, causing pneumonitis. Farmer's lung is caused by spores or fungi, pigeon breeder's lung by dried faecal proteins — both from repeated inhalational exposure.TMU Type III & IV Hypersensitivity deck Slide 10
11Which is a defining property of type IV hypersensitivity?
Answer: A
The three properties are a 24–72 hour delay, recruitment of macrophages, and no antibody or complement. The delay is itself evidence of the mechanism: there is no pre-formed effector, so T cells must be activated and cells must migrate.TMU Type III & IV Hypersensitivity deck Slide 20
12How long after the second antigen contact does a type IV reaction appear?
Answer: B
The delay is diagnostic. Types I, II and III are antibody-mediated and antibody is already present in a sensitized person, so they act within minutes to hours. Type IV must build its effector response from scratch.TMU Type III & IV Hypersensitivity deck Slides 20, 23
13Which cytokine activates macrophages in delayed-type hypersensitivity?
Answer: C
IFN-γ from Th1 cells is the principal macrophage-activating cytokine. TNF-α and TNF-β cause the local tissue injury and increase adhesion-molecule expression on endothelium. IL-4, IL-5 and IL-10 are Th2 cytokines and drive type I instead.TMU Type III & IV Hypersensitivity deck Slide 24
14A negative tuberculin (OT) test at 72 hours may indicate:
Answer: D
The three stated causes are: the vaccine has lost efficacy; the patient never contacted the bacterium; or immunodeficiency. The test does not detect the organism — it detects the patient's T-cell response to it, so an anergic patient tests negative however much organism is present.TMU Type III & IV Hypersensitivity deck Slide 29
15Contact dermatitis to nickel occurs because nickel:
Answer: A
Nickel is far too small to be immunogenic alone — the textbook hapten from Unit 2. Binding keratin supplies the carrier, exactly as penicillin binding serum albumin did. Same principle, different outcome: penicillin's conjugate drives IgE and type I; nickel's drives T cells and type IV.TMU Type III & IV Hypersensitivity deck Slide 30
16Which pairing of Th subset and hypersensitivity type is correct?
Answer: B
Th1 → type IV (IFN-γ activates macrophages for the delayed reaction); Th2 → type I (IL-4 drives class switching to IgE). This is True/False Q11, and it is the Unit 5 Th1/Th2 table applied clinically.Past Papers 2019 & 2020, Section IV Q11 · TMU Type III & IV Hypersensitivity deck Slide 24
1 Type III hypersensitivity — 3 marks+
Immune-complex hypersensitivity. Soluble antigen and antibody form complexes; medium-sized complexes (≈19S), formed at an appropriate antigen:antibody ratio, are too small to be phagocytosed and too large to be filtered by the glomerulus, so they deposit in local sites — joint synovium, glomerular basement membrane, choroid plexus — and activate complement strongly, recruiting neutrophils that release lytic enzymes.TMU Type III & IV Hypersensitivity deck Slides 3–8
2 Type IV hypersensitivity (DTH) — 3 marks+
Delayed-type hypersensitivity, with three defining properties: ① delay of 24–72 hours after the second antigen contact; ② recruitment of macrophages; ③ no antibody and no complement involved. Mediated by effector CD4⁺ Th1 (secreting IFN-γ to activate macrophages, and TNF-α/β causing local tissue injury) and effector CD8⁺ CTL (killing target cells directly).TMU Type III & IV Hypersensitivity deck Slides 20–24
3 Arthus reaction — 3 marks+
An experimental local immune-complex disease (1903) occurring at a small blood vessel wall. An animal repeatedly immunised subcutaneously with horse serum develops oedema, erythema and even necrosis. The human equivalent is the Arthus-like reaction at the site of repeated insulin injection in a type 1 diabetic.TMU Type III & IV Hypersensitivity deck Slide 9
4 Serum sickness — 3 marks+
A systemic immune-complex disease. When large amounts of antiserum — anti-tetanus or anti-diphtheria — enter an individual, 1–2 weeks later they develop fever, weakness and vasculitis. Antigen and antibody meet in the circulation at the mid-range ratio, forming exactly the medium-sized complexes that deposit.TMU Type III & IV Hypersensitivity deck Slide 11
5 Rheumatoid factor — 3 marks+
The auto-antibody of rheumatoid arthritis: an IgM anti-IgG antibody directed against degenerated IgG. The resulting immune complexes deposit in the synovium of small joints, producing symmetric, progressive, destructive lesions and eventual deformity.TMU Type III & IV Hypersensitivity deck Slide 14
1Immune-complex disease is caused by ? -sized complexes, which are too ? to be phagocytosed and too ? to be filtered by the glomerulus.3 mark(s)
Large complexes are cleared fast by phagocytes; small ones pass into the urine and do not fix complement. Only the middle size is trapped where it can do harm.
TMU Type III & IV Hypersensitivity deck Slide 42Immune complexes characteristically deposit in the ? of joints, the ? of the kidney, and the ? of the brain.3 mark(s)
All three filter blood under pressure through small vessels.
TMU Type III & IV Hypersensitivity deck Slide 33In type III hypersensitivity, ? , ? and ? act as chemotactic factors recruiting neutrophils.3 mark(s)
The recruited neutrophils then release lytic enzymes, which cause most of the tissue damage.
TMU Type III & IV Hypersensitivity deck Slide 64The three properties of type IV hypersensitivity are a delay of ? hours, recruitment of ? , and the involvement of no ? and no ? .4 mark(s)
The delay is itself evidence that no antibody is involved — there is no pre-formed effector waiting.
TMU Type III & IV Hypersensitivity deck Slide 205In type IV hypersensitivity, ? activates macrophages while ? and ? cause local tissue injury.3 mark(s)
All are Th1 cytokines — which is why Th1 drives type IV and Th2 drives type I.
TMU Type III & IV Hypersensitivity deck Slide 246A positive OT (tuberculin) test shows red induration about ? mm in diameter at ? hours.2 mark(s)
Contrast the type I skin test — wheal and flare >5 × 5 mm at 30 minutes. The timing distinguishes the mechanisms.
TMU Type III & IV Hypersensitivity deck Slide 281Th1 cells are involved in Type IV hypersensitivity and Th2 cells are involved in Type I hypersensitivity.
TRUE
TRUE — both halves. Th1 secretes IFN-γ, which activates macrophages and drives the delayed reaction; Th2 secretes IL-4, which drives class switching to IgE and so drives type I. The same Unit 5 knowledge answers this and the Th1/Th2 True/False trap.Past Papers 2019 & 2020, Section IV Q11 — verbatim, both years
2Antibody and complement are required for type IV hypersensitivity.
FALSE
False — and this is one of its three defining properties. Type IV is purely cell-mediated: CD4⁺ Th1 and CD8⁺ CTL, with macrophages recruited. The 24–72 hour delay is the clinical evidence of it.TMU Type III & IV Hypersensitivity deck Slide 20
3Large immune complexes are the most pathogenic.
FALSE
False. Large complexes are cleared rapidly by the phagocyte system and cause no damage. It is the medium-sized complexes that deposit and cause disease.TMU Type III & IV Hypersensitivity deck Slide 4
4A negative tuberculin test always means the patient has never been exposed to tuberculosis.
FALSE
False — a dangerous assumption. A negative test may also mean the vaccine has lost efficacy, or that the patient is immunodeficient and cannot mount the T-cell response. The test measures the response, not the organism.TMU Type III & IV Hypersensitivity deck Slide 29
5Delayed-type hypersensitivity is always detrimental to the host.
FALSE
False, and the deck says so explicitly: the term hypersensitivity is somewhat misleading. DTH is an important effector form of cell-mediated immunity — in essence, inflammation — and it is how intracellular organisms such as tuberculosis are contained. The granuloma is both tissue damage and successful containment.TMU Type III & IV Hypersensitivity deck Slide 39
6Serum sickness is a type III hypersensitivity reaction.
TRUE
True. Large amounts of horse antiserum provoke antibody while the horse protein is still circulating; antigen and antibody meet in the blood at the mid-range ratio, forming medium-sized complexes. Symptoms — fever, weakness, vasculitis — appear 1–2 weeks later.TMU Type III & IV Hypersensitivity deck Slide 11
1
Explain the mechanism of type III hypersensitivity.
6 marks
Formation and size. Soluble antigen stimulates antibody; immune complexes form. Their fate depends on size:
| Small | Medium (≈19S) | Large | |
|---|---|---|---|
| Complement activation | − | +++ | +++ |
| Clearance | Filtered by glomerulus | Deposits; difficult to remove | Cleared by phagocytes, fast |
| Damage | − | Causes immune complex disease | − |
Deposition sites. Joint synovium, glomerular basement membrane, choroid plexus — all filter blood under pressure through small vessels.
Injury. Deposited complexes activate complement. C3a, C4a, C5a (anaphylatoxins) degranulate mast cells and increase vascular permeability; C3a, C5a, C5b67 (chemotactic) recruit neutrophils, which release lytic enzymes; C3b activates platelets, giving aggregation and microthrombi. The result is oedema, haemorrhage and tissue damage.
Marking guide: 2 marks for the size rule, 1 for deposition sites, 3 for the complement and neutrophil mechanism. Stating that the neutrophil does the damage is the discriminating point.
2
Describe type IV hypersensitivity and its common diseases.
6 marks
Properties. ① Delay of 24–72 hours after the second antigen contact. ② Recruitment of macrophages. ③ No antibody and no complement involved.
Mechanism. Intracellular bacteria, viruses, parasites or chemicals are taken up by APCs; T cells differentiate into effector CD4⁺ Th1 and CD8⁺ CTL plus memory cells. On re-exposure, Th1 cells secrete chemokines (recruiting macrophages), IFN-γ (activating macrophages) and TNF-α/TNF-β (local tissue injury, increased endothelial adhesion molecules); CTLs lyse target cells directly.
Diseases. ① Infectious DTH — tuberculosis: first infection may give miliary TB, second gives a localised reaction, repeated occurrence gives chronic granuloma. The OT (tuberculin) test shows red induration ~5 mm at 24–48 h; a negative result may mean no exposure or immunodeficiency. ② Contact dermatitis — a hapten (nickel, dye, cosmetics, leather) binds keratin of the cuticle to form the antigen; effector T cells produce local red swelling and blistering.
Note: DTH is an important effector form of cell-mediated immunity — essentially inflammation — and is how intracellular organisms are contained.
Marking guide: 2 marks for the three properties, 2 for the mechanism with named cytokines, 2 for the two disease groups.
3
Compare the four types of hypersensitivity.
6 marks
| Type I | Type II | Type III | Type IV | |
|---|---|---|---|---|
| Name | Anaphylactic / immediate | Cytotoxic | Immune complex | Delayed (DTH) |
| Mediator | IgE | IgG, IgM on cell surface | Immune complexes | T cells |
| Antigen | Soluble allergen | Cell-surface | Soluble | Intracellular microbes, chemicals |
| Effectors | Mast cells, basophils, eosinophils | Complement, macrophages, NK cells | Complement, neutrophils, platelets | Th1, CTL, macrophages |
| Th subset | Th2 | — | — | Th1 |
| Timing | Minutes | Hours | 1–3 weeks | 24–72 hours |
| Complement | No | Yes | Yes | No |
| Diseases | Asthma, rhinitis, anaphylaxis | Transfusion reaction, HDN | SLE, RA, serum sickness | Contact dermatitis, tuberculin reaction |
Two questions place any disease: is it antibody or T cell? (T cell, macrophages, granuloma or days of delay → type IV); then where is the antigen? (on a mast cell via IgE → I; fixed on a target cell → II; soluble and forming deposits → III).
Marking guide: 0.75 per row. The mediator and antigen-location rows are essential; the Th subset row answers True/False Q11 at the same time.