Sunday, December 21, 2008

Pathophysiology of acute response allergy

So here you go, a lecture for the hypersentivity I for you. Haha!

When an allergen is encountered for the first time, it causes a response in TH2 lymphocyte, and produced interleukin-4 (IL-4). (Types of cytokines). These TH2 cells interact with B cells, through MHC II and costimulatory molecules CD40, CD80 and CD86). Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FcεRI) on the surface of mast cells and basophils, both involved in the acute inflammatory response. The IgE-coated cells, at this stage are sensitized to the allergen.

 

A later exposure by the same allergen causes reactivation of these IgE, which then signal for the degranulation of the sensitized mast cell or basophil. These granules release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction.

This results in the previously described symptoms of rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (calliscal anaphylaxis), or localised to particular body systems (for example, asthma to the respiratory system; eczema to the dermis).

 

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