Allergic response Causes of food allergies can result from three mechanisms of the allergic response: • IgE-mediated (classic) – the most common type, manifest as acute changes that occur within minutes to an hour or two after eating, and may progress to
anaphylaxis • Non-IgE mediated – characterized by an immune response not involving
immunoglobulin E; may occur hours to days after eating • IgE and non-IgE-mediated – a hybrid of the above two types
Allergic reactions are hyperactive responses of the immune system to substances that are innocuous to the majority of the population, such as food proteins. Why some proteins trigger allergic reactions while others do not is not entirely clear. One theory holds that proteins which resist digestion in the stomach, therefore reaching the small intestine relatively intact, are more likely to be allergenic. Some studies have shown that digestion may abolish, decrease, have no effect, or even increase the allergenicity of food allergens. The heat of cooking structurally degrades protein molecules, potentially making them less allergenic. In the early stages of acute allergic reaction,
lymphocytes previously sensitized to a specific sesame protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE). This type of antibody circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called
mast cells and
basophils. Both of these are involved in the acute inflammatory response. Activated mast cells and basophils undergo a process called
degranulation, during which they release
histamine and other inflammatory chemical mediators called (
cytokines,
interleukins,
leukotrienes, and
prostaglandins) into the surrounding tissue. These mediators on release cause several systemic effects, such as vasodilation,
mucous secretion,
nerve stimulation, and
smooth-muscle contraction. Cytokines from mast cells may also play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils.
Allergenic proteins Eight sesame seed allergens have been characterized (Ses i 1 to Ses i 8). Ses i 1 and Ses i 2 are of the biochemical type 2S
albumins; these partially share amino acid sequence and structure with 2S albumins from other plants, and are likely the proteins responsible for cross-reactive allergic reactions to peanuts and certain tree nuts, specifically almonds and hazelnuts. Ses i 3 is a
vicilin-like
globulin. Ses i 4 and Ses i 5 are
oleosins, associated with oil bodies, which appear to contribute to cross-reactivity to hazelnut and peanut oils. Allergic reactions to oleosins from sesame,
hazelnut and peanut oils have been confirmed, ranging from contact
dermatitis to
anaphylactic shock. The sesame oil body associated proteins are at ~17 and ~15 kDa, named, respectively, Ses i 4 and Ses i 5. Standardized sesame extracts used for allergy diagnosis do not contain oleosins, so the results of skin prick tests can present a false negative whereas using freshly ground seeds elicits a true positive. Commercial-grade peanut oil is highly refined, so the oleosins are removed, but commercial-grade sesame oil intended for food consumption is typically an unrefined product with a measurable protein content. ==Diagnosis==