Step by Step
I
Type I — Anaphylactic (immediate)
IgE, already bound to mast cells, encounters an allergen, triggering immediate degranulation and histamine release — reactions occur within minutes. Presents as urticaria, bronchoconstriction, or anaphylaxis, treated with epinephrine. Examples: peanut allergy, bee sting, latex allergy.
II
Type II — Cytotoxic
IgG or IgM binds directly to a cell surface, triggering complement activation or antibody-dependent cellular cytotoxicity (ADCC) that destroys the cell — occurring over hours. Examples: hemolytic disease of the newborn (Rh incompatibility), Goodpasture's syndrome, myasthenia gravis, Graves' disease.
III
Type III — Immune complex
Antigen-antibody complexes deposit in tissues, triggering complement activation and inflammation — occurring over days. Examples: serum sickness, systemic lupus erythematosus (SLE), post-streptococcal glomerulonephritis, rheumatoid arthritis.
IV
Type IV — Delayed (T cell-mediated)
No antibodies are involved — sensitized T cells drive the response, which takes 48-72 hours to develop. Examples: contact dermatitis, the TB skin test (PPD), transplant rejection, multiple sclerosis, and Type 1 diabetes.
Applied Walkthrough
1
A patient with a severe peanut allergy eats a small amount of peanut, and within minutes, IgE already bound to their mast cells triggers rapid degranulation — histamine release causes hives, bronchoconstriction, and potentially anaphylaxis, treated urgently with epinephrine. This is Type I hypersensitivity.
2
A different patient develops hemolytic disease of the newborn: maternal IgG antibodies bind directly to fetal red blood cell surface antigens, triggering complement-mediated destruction over a period of hours — this is Type II hypersensitivity.
3
A third patient develops post-streptococcal glomerulonephritis, weeks after a strep infection, as antigen-antibody complexes deposit in the kidney's glomeruli, triggering complement activation and inflammation over several days — this is Type III hypersensitivity.
4
A fourth patient develops contact dermatitis after touching poison ivy, with the reaction taking 48-72 hours to fully develop, driven entirely by sensitized T cells rather than antibodies — this delayed timeline and T cell mechanism define Type IV hypersensitivity.
Exam Application
Exams test whether you can match a given clinical scenario to the correct hypersensitivity type based on both timing (minutes, hours, days, or 48-72 hours) and mechanism (IgE, IgG/IgM, immune complexes, or T cells), and whether you know the classic disease examples for each type.
⚠ Common Trap
The most common trap is confusing Type II and Type III — both involve antibodies, but Type II involves antibodies binding directly to a specific cell's surface, while Type III involves antibody-antigen complexes that form elsewhere and then deposit in tissues, causing more diffuse inflammation.
✓ Quick Self-Check
1. What mediates Type I hypersensitivity, and how quickly does it occur?
IgE bound to mast cells; it occurs within minutes.
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2. What mediates Type II hypersensitivity?
IgG or IgM binding directly to a cell surface, triggering complement or ADCC.
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3. What mediates Type III hypersensitivity?
Antigen-antibody immune complexes depositing in tissues.
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4. What mediates Type IV hypersensitivity, and how long does it take to develop?
Sensitized T cells (no antibodies); it takes 48-72 hours.
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5. Give an example of a Type IV hypersensitivity reaction.
Any one of: contact dermatitis, TB skin test (PPD), transplant rejection, multiple sclerosis, Type 1 diabetes.
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