Hypersensitivity types I to IV

5 ASCP MLS practice questions on Hypersensitivity types I to IV, part of Immunology. The first 5 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

1. Question 1 · Hard

   A 30-year-old collapses with wheezing and hypotension 10 minutes after a wasp sting. Serum tryptase 1 hour later is 21 ng/mL [21 µg/L]; his baseline tryptase a week later is 6 ng/mL [6 µg/L]. How should these results be interpreted?

   1. AMast cell activation confirming anaphylaxis
   2. BAn invalid result drawn too late after onset
   3. CSystemic mastocytosis from a high baseline
   4. DA complement-mediated reaction, not mast cells

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   Answer: A · Mast cell activation confirming anaphylaxis

   Tryptase is released from mast cell granules and peaks about 1 to 2 hours after the reaction starts, so a 1-hour sample is well timed. A widely used rule calls a rise significant if the acute value exceeds 1.2 x baseline + 2 ng/mL: 1.2 x 6 + 2 = 9.2 ng/mL, and 21 ng/mL is well above this. The result confirms mast cell activation, as in IgE-mediated (type I) venom anaphylaxis. Venom-specific IgE testing can then identify the insect.

   • B: Tryptase peaks 1 to 2 hours after onset, so a 1-hour sample is ideal.
   • C: A baseline of 6 ng/mL is normal; mastocytosis is suggested by a persistently high baseline.
   • D: A raised tryptase points to mast cells, which is what defines this reaction.

2. Question 2 · Easy

   An itchy, blistering rash appears under a metal watch buckle two days after the wearer starts using the watch again. Which type of hypersensitivity is this nickel reaction?

   1. AType I (IgE-mediated)
   2. BType IV (T cell-mediated)
   3. CType II (cytotoxic antibody)
   4. DType III (immune complex)

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   Answer: B · Type IV (T cell-mediated)

   Nickel acts as a hapten: it binds skin proteins, and skin dendritic cells present the new antigen to T cells. On later contact, memory T cells release cytokines and recruit macrophages, so the rash takes 48 to 72 hours to appear. No antibody is involved, which is why the reaction is confirmed by patch testing rather than a blood test. Contact dermatitis and the tuberculin skin test are the classic type IV examples.

   • A: IgE reactions appear within minutes, as hives or wheezing, not after two days.
   • C: Type II reactions need antibody against a cell-surface or tissue antigen.
   • D: Type III reactions come from antigen-antibody complexes and complement, not T cells.

3. Question 3 · Medium

   Ten days after horse-derived antivenom for a snakebite, a man has fever, a rash, painful joints and proteinuria. Serum C3 and C4 are low. The mechanism that best explains this is:

   1. AImmune complexes depositing in vessels
   2. BIgE-triggered mast cell degranulation
   3. CAntibody binding to the patient's own cells
   4. DSensitized T cells releasing cytokines

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   Answer: A · Immune complexes depositing in vessels

   This is serum sickness, a type III reaction. Over one to two weeks the patient makes antibody to the foreign horse proteins while they are still circulating, so soluble complexes form in slight antigen excess. The complexes lodge in small vessels, glomeruli and joints and activate complement, which is why C3 and C4 fall. Symptoms settle once the foreign protein is cleared.

   • B: An IgE reaction would start within minutes of exposure and would not consume complement.
   • C: Type II reactions target fixed antigens, as in autoimmune hemolytic anemia.
   • D: T-cell reactions do not involve antibody or lower C3 and C4.

4. Question 4 · Medium

   On direct immunofluorescence of a kidney biopsy, smooth linear IgG along the glomerular basement membrane indicates:

   1. AComplement deposition with no antibody
   2. BAntibody to a basement membrane antigen
   3. CIgA complexes deposited in the mesangium
   4. DCirculating immune complexes that lodged there

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   Answer: B · Antibody to a basement membrane antigen

   A smooth linear pattern means antibody is bound evenly to an antigen that is part of the membrane itself. In anti-GBM disease (Goodpasture syndrome), IgG targets type IV collagen, a type II mechanism. Complexes trapped from the circulation give a lumpy, granular pattern instead, as in post-streptococcal glomerulonephritis or lupus nephritis (type III). A serum anti-GBM antibody assay supports the diagnosis.

   • A: C3 glomerulopathy shows complement with little or no immunoglobulin.
   • C: IgA nephropathy shows IgA in the mesangium, not linear IgG along the membrane.
   • D: Trapped immune complexes give a granular, lumpy pattern, not a linear one.

5. Question 5 · Easy

   What mediates type I (immediate) hypersensitivity?

   1. AImmune complex deposition
   2. BIgG or IgM against cell surface antigens
   3. CSensitized T lymphocytes
   4. DIgE bound to mast cells and basophils

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   Answer: D · IgE bound to mast cells and basophils

   In type I hypersensitivity, allergen cross-links IgE on mast cells and basophils, releasing histamine and other mediators within minutes. Examples include allergic rhinitis, asthma and anaphylaxis. Total and allergen-specific IgE help investigate it. Tryptase can confirm mast cell activation after anaphylaxis.

   • A: Immune complex disease is type III, as in serum sickness.
   • B: IgG or IgM against cells is type II, as in hemolytic transfusion reactions.
   • C: T-cell mediated reactions are type IV, as in the tuberculin test.