Pathology Cheat Sheet
Four Routes to Immune Injury
Hypersensitivity reactions for NEET-PG: type I IgE anaphylaxis, type II antibody-mediated, type III immune complex, and type IV delayed T-cell reactions.
MedNext Academy | 3 min read
Four Routes to Immune Injury
Hypersensitivity reactions for NEET-PG: type I IgE anaphylaxis, type II antibody-mediated, type III immune complex, and type IV delayed T-cell reactions.
The four types of hypersensitivity reactions and the immune mechanisms and diseases characteristic of each.
High-yield lines
- Type I hypersensitivity is IgE-mediated, causing mast cell degranulation with histamine and leukotriene release within minutes.
- Type I reactions cause anaphylaxis, asthma, allergic rhinitis, atopic dermatitis, and urticaria.
- Type II hypersensitivity is antibody-mediated, in which IgG or IgM binds cell-surface antigens causing complement activation, phagocytosis, or receptor dysfunction.
- Type II diseases include autoimmune haemolytic anaemia, Goodpasture disease, Graves disease, myasthenia gravis, and pemphigus.
- Type III hypersensitivity is immune-complex-mediated, depositing antigen-antibody complexes that activate complement and recruit neutrophils.
- Type III diseases include serum sickness, the Arthus reaction, and immune-complex glomerulonephritis.
- Type IV hypersensitivity is delayed and T-cell-mediated, without antibody, developing over 48 to 72 hours.
- Type IV reactions include the tuberculin test, contact dermatitis, and granulomatous inflammation.
- Graves disease is a type II reaction where antibodies stimulate the TSH receptor, and myasthenia gravis blocks the acetylcholine receptor.
- The Arthus reaction is a localised type III reaction from immune complexes in the vessel wall.
- Many real diseases combine mechanisms, as SLE involves both type II and type III injury.
- Type IV granulomatous hypersensitivity is driven by Th1 cells and activated macrophages.
Mapped competency codes
- PA9.2
Continue into the full chapter
This summary maps to PA9-immunopathology-and-aids.
Frequently Asked Questions
What mediates type I hypersensitivity?
IgE bound to mast cells cross-linked by antigen, triggering degranulation with release of histamine, leukotrienes, and prostaglandins within minutes, causing anaphylaxis and allergy.
How does type II hypersensitivity injure tissue?
IgG or IgM antibody binds cell-surface or matrix antigens, causing damage through complement activation, opsonisation and phagocytosis, or interference with receptor function.
What characterises type IV hypersensitivity?
A delayed T-cell-mediated reaction without antibody, developing over 48 to 72 hours, seen in the tuberculin test, contact dermatitis, and granuloma formation.
Which hypersensitivity type causes serum sickness?
Type III, in which circulating antigen-antibody immune complexes deposit in tissues, activate complement, and recruit neutrophils that cause injury.
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