Food allergies, including immediate hypersensitivity reactions involving IgE and other, delayed hypersensitivity reactions involving other immunoglobulins, contribute to immunemediated tissue injury and disease. IgE antibodies are thought to trigger allergic reactions when cross-linking occurs on GI mast cells, resulting in a cascade of histamines and leukotrienes. Histamine-receptor activation is one possible mechanism for underlying cellular pathways that cause the barrier function of the intestinal epithelium to break down.13 The onslaught of previously mentioned inflammatory allergic molecules and their alteration of intestinal permeability permit food macromolecules to pass through the mucosal serosa. Once food antigens are in circulation, they may predispose other organs and systems of the body to allergic reactions.
In addition, IgG antibodies have been shown, experimentally, to increase the permeability of the intestinal wall.14 Increased intestinal permeability has been indicated as a precipitating factor in allergic diseases, such as chronic urticaria.15 The majority of food allergies are IgE-mediated, and the amount of evidence on this immunoglobulin as a marker for food allergy is extremely large and is increasingly more common. However, the significance of food-specific serum IgG4 antibody in food allergy is unclear, although concomitant elevations of both IgE and IgG are found in various food allergies.16 This does not imply, necessarily, that these IgG levels are causing the allergy symptoms, but rather that IgG is somehow involved in the allergy process.
Although IgGs are present in the food-allergy reaction, it is unknown if these antibodies are contributing to the allergic process and concomitant symptomatology or if they provide a type of blocking mechanism against IgE antibodies involved in the allergic process. For example, two common food allergens, peanut and ovalbumin, elicit specific IgG antibody responses that are measured using enzyme-linked immunosorbent assays (ELISAs) as well as testing for IgE responses.17 It has been suggested, however, that IgG is responsible for long-term reactivity to allergens because of the extended life of IgG antibodies in the serum. IgE has a half-life of only 1 to 2 days (in circulation) while mast-cell-committed IgE has an approximate half-life of 14 days. Alternatively, IgG has a half-life of approximately 21 days in circulation, with a half-life on bound mast cells of 2 to 3 months.18 The conventional radioallergosorbent test (RAST) and skin testing of food allergies are not wholly adequate for diagnosing an IgG-related allergy because these tests mainly reveal the presence of IgE-related allergies.
Once food antigens are in circulation, they may predispose other organs and systems of the body to allergic reactions.
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