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Hypersensitivity Reactions Quiz
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Which immunological mechanism best characterises a type I hypersensitivity reaction?
- A IgE-mediated mast cell degranulation following re-exposure to an antigen You picked ✓
- B Delayed macrophage activation driven by Th1 lymphocytes You picked ✕
- C Immune complex deposition in tissues leading to inflammation You picked ✕
- D IgG or IgM antibodies binding to cell surface antigens causing complement activation You picked ✕
- E T-cell mediated cytotoxicity against infected host cells You picked ✕
Correct!
Incorrect
The answer is A: IgE-mediated mast cell degranulation following re-exposure to an antigen
Explanation
Why A is correct
See Type I Hypersensitivity. Option A is correct. Type I hypersensitivity is the immediate, allergic type of reaction. On the first exposure to an allergen (a harmless substance such as pollen or peanut that provokes allergy), the immune system makes allergen-specific IgE antibodies, which attach to mast cells and basophils (cells packed with chemical mediators). This is the sensitisation step, and nothing is felt. On a later exposure, the allergen cross-links the IgE on the cell surface, which makes the cell release its contents (degranulation). The mediators include histamine, which widens blood vessels and makes them leaky, and leukotrienes, which tighten the airways. The result appears within minutes, usually within about 30 minutes, and can be local, such as hay fever or urticaria, or body-wide, as in anaphylaxis. A helpful reminder is the ABCD method, in which type I is the Allergic type. Whenever you see IgE, mast cells and an immediate onset, think type I.
- Type I is Allergic (immediate, IgE and mast cells)
- Type II is antiBody-mediated (antibodies against cell-bound antigens)
- Type III is immune Complex-mediated (antibodies with soluble antigens)
- Type IV is Delayed (T-cell mediated)
- Type: type I is the immediate, allergic type of hypersensitivity.
- Mechanism: on re-exposure the allergen cross-links IgE on mast cells, which degranulate.
- Mediators: histamine widens and leaks blood vessels and leukotrienes tighten the airways, within minutes.
Why the other options are incorrect
- B. Delayed macrophage activation driven by Th1 lymphocytes: Delayed macrophage activation driven by Th1 lymphocytes is also a type IV process, as in the tuberculin reaction. It develops over a day or more and not within minutes. It would be the answer to a question about a delayed T-cell reaction. Your answer
- C. Immune complex deposition in tissues leading to inflammation: Deposition of immune complexes in tissues is the hallmark of type III hypersensitivity. It causes inflammation hours to days later rather than within minutes. It would be the answer to a question about serum sickness. Your answer
- D. IgG or IgM antibodies binding to cell surface antigens causing complement activation: IgG or IgM binding to cell-surface antigens and activating complement is the type II mechanism. It destroys cells and is not an immediate allergic reaction. It would be the answer to a question about haemolytic disease or Goodpasture syndrome. Your answer
- E. T-cell mediated cytotoxicity against infected host cells: T-cell cytotoxicity against infected host cells is a type IV mechanism. It is slow and does not involve IgE or mast cells. It would be the answer to a question about delayed-type hypersensitivity. Your answer
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More questions from this set. Start the quiz to answer them and see each explanation.
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1
Which immunoglobulin class is responsible for causing haemolytic disease of the newborn in type II hypersensitivity reactions?
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2
Which sequence best describes the development of a hypersensitivity reaction?
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