Homepage | Imprint
Lumrix Logo
 
 
Lumrix Wiki Logo
[ICD 10 Search]



Back
[ICD 10 Search]

 

 

Hypersensitivity

Hypersensitivity is an immune responsethat damages the body's own tissues. Four or five types of hypersensitivity are often described. The four-group classification was expounded by P.H.G. Gelland Robin Coombsin 1968 (See Gell-Coombs classification.

Inhaltsverzeichnis

  • 1 Type I - immediate (or atopic, or anaphylactic)
  • 2 Type II - antibody-dependent (or cytotoxic)
  • 3 Type III - immune complex
  • 4 Type IV - cell-mediated (or delayed)
  • 5 Type V - stimulatory
  • 6 See also
  • 7 External links

Type I - immediate (or atopic, or anaphylactic)

Main article: Allergy

Type I hypersensitivity is an allergy reaction provoked by reexposure to a specific antigen. Exposure may be by ingestion, inhalation, injection, or direct contact. The reaction is mediated by IgEantibodiesand produced by the immediate release of histamine, arachidonateand derivatives by basophilsand mast cells. This causes an inflammatoryresponse leading to an immediate (within seconds to minutes) reaction.

The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock. Treatment usually involves epinephrine, antihistamines, and corticosteroids.

Some examples:

  • Allergic asthma
  • Allergic conjunctivitis
  • Allergic rhinitis("hay fever")
  • Anaphylaxis
  • Angioedema
  • Urticaria(hives)

Type II - antibody-dependent (or cytotoxic)

In type II hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). IgGand IgMantibodies bind to these antigens to form complexes that activate the classical pathwayof complementactivation for eliminating cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexescause cell lysis and death. The reaction takes hours to a day.

Another form of type II hypersensitivity is called Antibody Dependent Cell Mediated Cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by Natural Killer (NK) cells and macrophages (through the attached antibodies), which in turn kill these tagged cells.

Some examples:

  • Autoimmune haemolytic anaemia
  • Goodpasture's syndrome
  • Pemphigus
  • Pernicious anemia
  • Immune thrombocytopenia
  • Transfusionreactions

Type III - immune complex

In type III hypersensitivity, soluble immune complexes (aggregations of antigens and IgG and IgM antibodies) form in the bloodand are deposited in various tissues (typically the skin, kidneyand joints) where they may trigger an immune response according to the classical pathway of complement activation (see above). The reaction takes hours to days to develop.

Some clinical examples:

  • Immune complex glomerulonephritis
  • Rheumatoid arthritis
  • Serum sickness
  • Subacute bacterial endocarditis
  • Symptoms of malaria
  • Systemic lupus erythematosus
  • Arthus reaction

Type IV - cell-mediated (or delayed)

Main article: Cell mediated immunity

Type IV hypersensitivity is often called delayed type as the reaction takes two to three days to develop. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response.

CD8 cytotoxic T cellsand CD4 helper T cellsrecognise antigen in a complex with either type I or II major histocompatibility complex. The antigen-presenting cells in this case are macrophagesand they release interleukin1, which stimulates the proliferation of further CD4 cells. These cells release interleukin 2 and gamma interferon, which together regulate the immune reaction. Activated CD8 cells destroy target cells on contact while activated macrophages produce hydrolyticenzymesand, on presentation with certain intracellular pathogens, transform into multinucleated giant cells.

Some clinical examples:

  • Contact dermatitis(poison ivy rash, for example)
  • Hashimoto's thyroiditis
  • Diabetes mellitus type 1
  • Symptoms of leprosy
  • Symptoms of tuberculosis
  • Transplant rejection

Type V - stimulatory

This is an additional type that is sometimes (often in Britain) used as a distinction from Type II.

Instead of binding to cell surface components so the cells are destroyed, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligandbinding with the receptor or mimics the effects of the ligand, thus impairing cell signalling.

Some clinical examples:

  • Graves' disease
  • Myasthenia gravis

See also

  • Allergy

External links

  • Merck Manual12-148a
  • DDB28827
  • eMedicinemed/1101
  • GPnotebook-529858552
  • FPnotebookENT45ia:Hypersensitivitate
Retrieved from "http://en.wikipedia.org/Hypersensitivity"



This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Hypersensitivity Wikipedia article Hypersensitivity.

 
  All text is available under the terms of the GNU Free Documentation License