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Mast cell - Physiology

Mast cell - Physiology: Encyclopedia II - Mast cell - Physiology

Mast cells express a high-affinity receptor (FcεRI) for Immunoglobulin E (IgE), the least abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is essentially irreversible. As a result, mast cells are coated with IgE. IgE is, in turn, synthetised by B-cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific for one specific epitope. In allergic reactions, mast cells remain inactive until an allergen binds to IgE already in association ...

See also:

Mast cell, Mast cell - Origin and classification, Mast cell - Physiology, Mast cell - Role in disease, Mast cell - Allergic disease, Mast cell - Anaphylaxis, Mast cell - Mast cell disorders, Mast cell - Sources

Mast cell, Mast cell - Allergic disease, Mast cell - Anaphylaxis, Mast cell - Mast cell disorders, Mast cell - Origin and classification, Mast cell - Physiology, Mast cell - Role in disease, Mast cell - Sources

Mast cell: Encyclopedia II - Mast cell - Physiology



Mast cell - Physiology

Mast cells express a high-affinity receptor (FcεRI) for Immunoglobulin E (IgE), the least abundant member of the antibodies. This receptor is of such high affinity that binding of IgE molecules is essentially irreversible. As a result, mast cells are coated with IgE. IgE is, in turn, synthetised by B-cells (the antibody-producing cells of the immune system). IgE molecules, like all antibodies, are specific for one specific epitope.

In allergic reactions, mast cells remain inactive until an allergen binds to IgE already in association with the cell (see above). Allergens are generally proteins or polysaccharides. The allergen binds to the Fab part of the IgE molecules on the mast cell surface. It appears that binding of two or more IgE molecules (this is called crosslinking) is required to activate the mast cell; the steric changes lead to a slight disturbance to the cell membrane structure, causing a complex sequence of reactions inside the cell that lead to activation of the cell. Although this reaction is most well understood in terms of allergy, it appears to have evolved as a defense system against intestinal worm infestations (tapeworms, etc).

When activated, a mast cell rapidly releases its characteristic granules and various hormonal mediators into the interstitium. Other forms of activation besides IgE (such as by the complement system) have been described.

The molecules thus released into the intercellular environment include:

  • preformed mediators (from the granules):
    • histamine (2-5 pg/cell)
    • proteoglycans, mainly heparin (active as anticoagulant)
    • serine proteases
  • newly formed lipid mediators (eicosanoids)
    • prostaglandin D2
    • leukotriene C4
  • cytokines

Histamine dilates blood vessels, makes them leaky, and activates the endothelium. This leads to local edema (swelling), warmth, redness, and the attraction of other inflammatory cells to the site of release. It also irritates nerve endings (leading to itching or pain). Cuteanous signs of histamine release are the "flare and wheal"-reaction. The bump and redness immediately following a mosquito bite are a good example of this reaction, which occurs seconds after challenge of the mast cell by an allergen.

The other physiologic activities of mast cells are much less well understood. Several lines of evidence suggest that mast cells may have a fairly fundamental role in innate immunity -- they are capable of elaborating a vast array of important cytokines and other inflammatory mediators, they express multiple "pattern recognition receptors" thought to be involved in recognizing broad classes of pathogens, and mice without mast cells seem to be much more susceptible to a variety of infections. These cytokines and other mediators clearly also come into play during injury and wound healing.




Adapted from the Wikipedia article "Physiology", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki

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