Basophils triggering

Once sensitivity has been established, that is, once hapten-specific IgE-producing B cells have been formed, exposure to even small amounts of hapten can induce a cascade of events that lead to immediate reactions, such as anaphylaxis (210). Briefly, preformed IgE antibodies to drug determinants recognize the hapten-carrier complex and fix to the surface of mast cells or basophils, triggering the release of a series of mediators, such as histamine, neutral proteases, biologically active arachidonic acid products, and cytokines. This ultimately leads to a clinical spectrum that ranges from a mUd local reaction to anaphylactic shock. 

Anaphyla. is is a type I reaction in which the drug ( ) interacts with IgE lixed to mast cells contrast media) can produce an anaphylaxis-like (anaphylactoid) reaction on first exposure. 

There are also other immimological mechanisms, especially via IgG or IgM antibodies with immune complex formation, which can lead to similar clinical conditions [20, 34, 42] as has been shown in dextran anaphylaxis (table 1). Triggering of mast cells and basophils leads to release of various vasoactive mediators, among which histamine was the first recognized in 1908 (fig. 3,4) [6]. 

The detection of reactions mediated by specific IgE to agents triggering anaphylaxis may be achieved by means of serological methods serum-specific IgE, or by means of cellular tests which determine the release of basophil mediators (leukotrienes and histamine) or by means of the analysis of basophil expression markers, a technique known as the basophil activation test (BAT). 

Somatostatin (SOM), initially identified by its ability to inhibit the release of growth hormone, is known to have inhibitory effects on a variety of cells [ 109], In mast cells and in basophils, SOM, like NT, has inhibitory as well as stimulatory effects depending on the concentration used. At high concentrations (> 10 8 M), SOM is a powerful stimulus of peritoneal mast-cell secretion (from both normal and athymic rats) and resembles other non-immunologic secretagogues such as compound 48/80, SP and NT in that it triggers a rapid exocytosis that is primarily dependent on cellular Ca [ 110,111], A similar effect is seen in vivo when injected into skin or skin blisters at high concentrations (> 10-8 M), SOM causes a rapid, dose-dependent release of histamine [88, 112] but when used at concentrations lower than those which elicit a secretory... 

Most tissue histamine is sequestered and bound in granules (vesicles) in mast cells or basophils the histamine content of many tissues is directly related to their mast cell content. The bound form of histamine is biologically inactive, but as noted below, many stimuli can trigger the release of mast cell histamine, allowing the free amine to exert its actions on surrounding tissues. Mast cells are especially rich at sites... 

Allergen cross-links IgE on mast cell (or basophil) and triggers degranulation and release of pharmacologic mediators... 

Gao Z, Li BS, Day YJ, Linden J (2001) A3 adenosine receptor activation triggers phosphorylation of protein kinase B and protects rat basophilic leukemia 2H3 mast cells from apoptosis. Mol Pharmacol 59 76-82... 

Davenas E, Beauvais J, Amara J, Oberbaum M, Robinzon B, Miadonna A, Tedeschi A, Pomeranz B, Fortner P, Belon P, Sainte-Laudy J, Poitevin B, Benveniste J. 1988. Human basophil degranulation triggered by very dilute antiserum against IgE. Nature 333 816-818. 

IgEMonomer Binds to allergens and triggers histamine release from mast cells and basophils also protects against parasitic worms. 

HRF is one of the many immune system protein molecules called cytokines that trigger allergic reactions. Unlike other cytokines, HRF stimulates basophils to release histamine (MacDonald, 1996). 

---