by Mark Lin

Created on: December 18, 2008

Allergy, the condition of developing red spots, itchiness, etc, may be medically defined as the hypersensitivity reaction type I. In this type of hypersensitivity reaction, various stimuli from the environment may be potent to trigger the release of histamine, the underlying cause of allergy, from the corresponding cells by the mechanisms discussed below.

In hypersensitivity reaction type one, histamine is released from basophils and mast cells in a process known as anaphlaxis. First of all, the stimulant of the reaction from the external environment, known as the allergen, is presented to the host. The host dendritic cells, a specific kind of antigen presenting cell (APC) on the skin, presents the allergen to the CD4+ T cells. The CD4+ T cells (more specifically TH2 subgroup of the kind) then secrete the chemokine known as interleukin 5, abbreviated IL-5. The function of interleukin five is to recruit eosinophils, the star of allergic reactions, from the blood stream to the site of exposure. Upon migration, the eosinophils then secrete immunoglobulin E (IgE). The immunoglobulin E acts on the local mast cells and basophils to release histamine from the cellular cytoplasmic granules. (p. 208 Robbin's Basis of Disease) Aside from releasing histamine, a wide variety of the substances are co-released into the site of exposure. Substances such as cytokines and lipid mediators are exocytosed in secondary granules (with histamine being in the primary granule).

Allergic reactions may be divided into two phases, an early phase and a late phase. In the early phase, vascular changes predominate. Owing to histamine's virtue as a potent vasodilator and agent increasing the vascular permeability, one may be able to observe local edema at the site of exposure of several degrees, ranging from modest to severe. Increased permeability results in leakage of blood filtrates into the interstitium of the local tissues, resulting in the appearance of such. Vasodilation of the blood vessels may be responsible for the appearance of red spots, due to the local hyperemia that has occurred. A final note must be made about the inflammatory response seen later in time after the exposure. The so called lipid-mediators facilitate the metabolsim of arachidonic acids, the precurser for numerous inflammatory agents, into leukotrienes and prostaglandins. Prostaglandins is produced in a biochemical reaction catalyzed by the enzyme cyclooxygenase, which has two isoforms. The first isoform is expressed continuously and maintains the normal body temperature. The second may be found in inflammatory reactions and accounts for the fever observed. Leukotriene functions simply as a chemokine that recruits immune cells of acute inflammation to the site of exposure. Among the immune cells one may observe numerous neutrophils if the biopsy of the tissue were performed. To conclude one may observed the above phenomenom due to the release of primary and secondary granules.

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