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PH-IM11

Hypersensitivity reactions

How the immune system harms the body it protects: IgE and mast cells (type I), antibodies against cells and tissue (type II), deposited immune complexes (type III) and sensitised T cells (type IV), with their timing and typical diseases.

By the end, you can

  • Classify hypersensitivity reactions into the four Gell and Coombs types by their mechanism.
  • Explain the sensitisation, early phase and late phase of a type I reaction.
  • Describe how antibodies against cells or tissue cause damage or change receptor function (type II).
  • Explain why immune complexes injure filtering vessels such as glomeruli (type III).
  • Explain why T-cell reactions are delayed, and how persistent ones form granulomas (type IV).
  • Recognise the tissue picture and tests of each type, and explain how antihistamines, adrenaline, glucocorticoids, desensitisation and antibody-directed treatments act on the mechanism.

What it is

Hypersensitivity is an immune response, to a foreign antigen or to the body’s own, that damages the host. The Gell and Coombs classification divides it by mechanism: type I (immediate; IgE and mast cells), type II (antibody against antigens on cells or tissue), type III (immune complexes deposited in tissue) and type IV (delayed; T cells). Many diseases involve more than one type.

4 types to tell apart
Type I (immediate)
IgE bound to mast cells is cross-linked by allergen, releasing mediators within minutes: hay fever, allergic asthma, food allergy, anaphylaxis.
Type II (antibody against cells or tissue)
IgG or IgM binds fixed antigens, causing phagocytosis, complement injury or altered receptor function: haemolytic disease of the newborn, anti-GBM disease, Graves disease.
Type III (immune complex)
Antigen–antibody complexes lodge in vessel walls and activate complement wherever they deposit: serum sickness, post-infectious glomerulonephritis, lupus.
Type IV (delayed, T-cell-mediated)
Sensitised T cells cause inflammation over 24–72 hours: contact dermatitis, the tuberculin reaction, granulomas.

Normal function

Targeted immunity and its effector cells

Adaptive immunity is aimed at microbes. Dendritic cells and present fragments of antigen to helper T cells, which direct the response: B cells mature into that secrete antibodies (IgM, IgG, IgA or IgE), and cytotoxic T cells kill infected cells.

Antibodies coat microbes for phagocytosis, activate complement and neutralise toxins. carry IgE on their surface and release histamine when it is cross-linked, which helps expel parasites. Memory cells make every later response faster and stronger.

The same tools cause disease when they are aimed at a harmless antigen, at the body’s own tissue, or used out of proportion. Which tool does the damage defines the four types of hypersensitivity.

Point to it on the model
The four types of hypersensitivitySchematic
FeatureWhat does the damageTimingExamples
Type I (immediate)IgE on mast cells and basophilsMinutes; late phase after hoursHay fever, allergic asthma, food allergy, anaphylaxis
Type II (antibody to cells or tissue)IgG or IgM, complement, phagocytesMinutes to daysHaemolytic disease of the newborn, anti-GBM disease, Graves disease, myasthenia gravis
Type III (immune complex)Antigen–antibody complexes, complement, neutrophilsHours (local) to 1–2 weeks (serum sickness)Serum sickness, post-infectious glomerulonephritis, lupus
Type IV (delayed, T cell)CD4 and CD8 T cells, macrophages24–72 hoursContact dermatitis, tuberculin reaction, granulomas, type 1 diabetes

Gell and Coombs classification, simplified; many diseases involve more than one type.