Type I: immediate hypersensitivity
IgE made at first exposure (sensitisation) binds to mast cells and basophils. On re-exposure to the same allergen these cells release histamine and other mediators, and symptoms appear within minutes. Examples: allergic rhinitis, asthma, urticaria, food and drug allergy, anaphylaxis. Tests: skin prick test, specific IgE.
Type II: cytotoxic hypersensitivity
IgG or IgM binds antigens on cell surfaces or in tissue and destroys cells or alters their function through complement, phagocytosis or antibody-dependent cytotoxicity. Examples: ABO-incompatible transfusion reactions, haemolytic disease of the newborn, autoimmune haemolytic anaemia, Goodpasture syndrome, Graves' disease (receptor-stimulating). Test: Coombs test.
Type III: immune complex hypersensitivity
Complexes of soluble antigen and antibody deposit in vessel walls, kidney glomeruli or joints, activate complement and cause inflammation. Examples: systemic lupus erythematosus, serum sickness, post-streptococcal glomerulonephritis, the Arthus reaction.
Type IV: delayed-type hypersensitivity
Sensitised T cells, not antibodies, drive the response, which appears 24–72 hours after exposure. Examples: the tuberculin skin test (PPD), contact dermatitis (poison ivy, nickel), part of transplant rejection, type 1 diabetes.
Study tips
- Remember the mediator: type I IgE, type II antibody against cell-bound antigen, type III immune complexes, type IV T cells.
- Real diseases can mix mechanisms, and recent textbooks subdivide type IV.
- For another case of runaway immune activation, see cytokine release syndrome.
References
- Gell, P. G. H., & Coombs, R. R. A. (Eds.). (1963). Clinical Aspects of Immunology. Blackwell Scientific.
- Abbas, A. K., Lichtman, A. H., & Pillai, S. (2021). Cellular and Molecular Immunology (10th ed.). Elsevier.
- Murphy, K., & Weaver, C. (2016). Janeway's Immunobiology (9th ed.). Garland Science.
- Kumar, V., Abbas, A. K., & Aster, J. C. (2020). Robbins & Cotran Pathologic Basis of Disease (10th ed.). Elsevier.