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Other names: Hypersensitivity reaction, intolerance

Hypersensitivity refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over-reaction of the immune system and these reactions may be damaging, uncomfortable, or occasionally fatal. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. The Gell and Coombs classification of hypersensitivity is the most widely used, and distinguishes four types of immune response which result in bystander tissue damage.[1]

Coombs and Gell classification

Immunologic aspects of hypersensitivity reactions
Type Alternative names Antibodies or Cell Mediators Immunologic Reaction Often mentioned disorders Videos
I Fast response which occurs in minutes, rather than multiple hours or days. Free antigens cross link the IgE on mast cells and basophils which causes a release of vasoactive biomolecules. Testing can be done via skin test for specific IgE.[2]
Video explanation of type I hypersensitivity
II Antibody (IgM or IgG) binds to antigen on a target cell, which is actually a host cell that is perceived by the immune system as foreign, leading to cellular destruction via the MAC. Testing includes both the direct and indirect Coombs test.[3]
Video explanation of type II hypersensitivity
III Antibody (IgG) binds to soluble antigen, forming a circulating immune complex. This is often deposited in the vessel walls of the joints and kidney, initiating a local inflammatory reaction.[4]
Video explanation of type III hypersensitivity
IV Cells T helper cells (specifically Th1 cells) are activated by an antigen presenting cell. When the antigen is presented again in the future, the memory Th1 cells will activate macrophages and cause an inflammatory response. This ultimately can lead to tissue damage.[5]
Video explanation of type IV hypersensitivity

This is an additional type that is sometimes (especially in the UK) used as a distinction from Type 2.[7]

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.[citation needed]


  1. 1.0 1.1 See type V explanation in table.


  1. "Davidson's Principles and Practice of Medicine, IE Edition, 20th Ed: Medicine—Clinical Medicine". Journal of Endocrinology, Metabolism and Diabetes of South Africa. 13 (2): 75–75. July 2008. doi:10.1080/22201009.2008.10872174. ISSN 1608-9677. Archived from the original on 2021-08-28. Retrieved 2020-02-13.
  2. 2.0 2.1 Black, C. A. (1999). "Delayed type hypersensitivity: Current theories with an historic perspective". Dermatology Online Journal. 5 (1): 7. PMID 10673450. Archived from the original on 2015-06-11. Retrieved 2015-05-15.
  3. 3.0 3.1 Delayed Hypersensitivity Reactions at eMedicine
  4. Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2014). "Hypersensitivity: Immunologicaly Mediated Tissue Injury". Robbins & Cotran Pathologic Basis of Disease (9th ed.). Elsevier Health Sciences. pp. 200–11. ISBN 978-0-323-29635-9. {{cite book}}: |access-date= requires |url= (help); |archive-url= requires |url= (help); Unknown parameter |chapterurl= ignored (help)
  5. Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204
  6. Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). "Table 5-1". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
  7. Rajan, T.V. (2003). "The Gell–Coombs classification of hypersensitivity reactions: A re-interpretation". Trends in Immunology. 24 (7): 376–9. doi:10.1016/S1471-4906(03)00142-X. PMID 12860528.

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