Hypersensitivity

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Hypersensitivity
Classification and external resources
ICD-10T78.4
ICD-9995.3
DiseasesDB28827
MeSHD006967
 
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This article is about the medical condition. For the music album, see Hypersensitive.
For the cause of dental pain, see Dentine hypersensitivity.
Hypersensitivity
Classification and external resources
ICD-10T78.4
ICD-9995.3
DiseasesDB28827
MeSHD006967

Hypersensitivity (also called hypersensitivity reaction or intolerance) is a set of undesirable reactions produced by the normal immune system, including allergies and autoimmunity. These reactions may be damaging, uncomfortable, or occasionally fatal. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. They are classified in four groups after the proposal of P. G. H. Gell and Robin Coombs in 1963.[1]

Coombs and Gell classification[edit]

Comparison of hypersensitivity types
TypeAlternative namesOften mentioned disordersMediatorsDescription
IAllergy (immediate)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]

IICytotoxic, antibody-dependentAntibody (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]

IIIImmune complex diseaseAntibody (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]
IVDelayed-type hypersensitivity,[2][3] cell-mediated immune memory response, antibody-independentHelper T cells (specifically Th1 helper t 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. [6]
VAutoimmune disease, receptor mediated (see below)

Type V[edit]

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

Instead of binding to cell surface components, 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.

Some clinical examples:

The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2.

See also[edit]

References[edit]

  1. ^ Gell PGH, Coombs RRA, eds. Clinical Aspects of Immunology. 1st ed. Oxford, England: Blackwell; 1963.
  2. ^ a b Black, CA. Delayed Type Hypersensitivity: Current Theories with an Historic Perspective Dermatol. Online J. (May 1999) 5(1):7 at http://dermatology.cdlib.org/DOJvol5num1/reviews/black.html
  3. ^ a b http://emedicine.medscape.com/article/136118-overview
  4. ^ Kumar, Vikay (2010). Robbins and Cotran pathologic basis of disease. (8th ed. ed.). Philadelphia, PA: Saunders/Elsevier. pp. 204–205. ISBN 9781416031215. 
  5. ^ Table 5-1 in:Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.
  6. ^ Le, Tau. First Aid for the USMLE Step 1 2013, p. 203-204
  7. ^ Rajan TV (July 2003). "The Gell-Coombs classification of hypersensitivity reactions: a re-interpretation". Trends Immunol. 24 (7): 376–9. doi:10.1016/S1471-4906(03)00142-X. PMID 12860528. 

External links[edit]