ABSTRACT
Allergic diseases, such as allergic asthma, are hypersensitivity reactions
initiated by immunological mechanisms (1,2). They are usually mediated
by IgE antibodies, triggering an inflammation characterized by an increase
in production of Th2-type cytokines at a mucosal surface, the interface between the external and the internal environments. Allergic diseases usually
occur in atopic individuals who are genetically predisposed to producing IgE
antibodies in response to low doses of general environmental allergens, e.g.,
pollens, mites, and danders. Although allergies mediated by other immuno-
globulins (e.g., IgG-immune complexes that can activate complement) or
lymphocytes (e.g., allergic contact dermatitis to chromium and nickel) also
exist, the major part, if not all, of allergic asthma is IgE mediated. The
cross-linking of mast cell/basophil membrane cell-bound IgE antibodies by allergen results in the release of inflammatory mediators that are responsible
for the signs and symptoms of allergy. IgE sensitization to an allergen can
develop in childhood or throughout life, and subsequent allergen contact,
which may occur years later, can initiate a severe attack of allergic asthma.
