Hypersensitivity
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hypersensitivity reactions types I II III IV Merck Manual
Hypersensitivity is an excessive or inappropriate immune response that causes tissue injury. The classic Gell and Coombs classification has four types. Merck Manual overview
| Type | Main mechanism | Typical timing | Examples |
|---|---|---|---|
| I - Immediate | Allergen-specific IgE binds mast cells/basophils. Re-exposure causes histamine and other mediator release. | Minutes | Anaphylaxis, allergic rhinitis, asthma, urticaria, food allergy |
| II - Antibody-mediated | IgG or IgM binds cell-surface or matrix antigens, causing complement activation, phagocytosis, or altered receptor function. | Hours to days | Autoimmune hemolytic anemia, transfusion reaction, Goodpasture syndrome, Graves disease |
| III - Immune complex-mediated | Circulating antigen-antibody complexes deposit in tissues and activate complement. | Usually days to weeks | Serum sickness, SLE, post-streptococcal glomerulonephritis, Arthus reaction |
| IV - Delayed, T-cell-mediated | Sensitized T lymphocytes cause macrophage activation or cytotoxic tissue damage. | 48-72 hours or longer | Contact dermatitis, tuberculin skin test, type 1 diabetes, graft rejection |
Type I sequence
- Initial exposure causes sensitization and IgE production.
- IgE attaches to mast cells.
- Re-exposure cross-links IgE.
- Mast cells release histamine, leukotrienes, prostaglandins, and cytokines.
- Effects include itching, edema, bronchospasm, mucus secretion, hypotension, and sometimes anaphylaxis.
A single illness can involve more than one mechanism. Drug reactions, for example, may be type I, II, III, or IV, and severe reactions such as Stevens-Johnson syndrome/toxic epidermal necrolysis require urgent medical assessment. Merck drug-hypersensitivity guidance
Source: Robbins & Kumar Basic Pathology, p. 141.
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