Type I IgETriggered Anaphylaxis

This type of immediate hypersensitivity reaction occurs within minutes in allergically sensitized individuals. Although serum IgE has a short half-life (one to two days), IgE antibodies bound to the Fce receptor on basophils

Kayser, Medical Microbiology © 2005 Thieme

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and mast cells have a half-life of several months and when bound by the specific allergen mediate cellular degranulation and the release of biogenic amines (e.g., histamine, serotonin). These mediators can influence the smooth musculature, and mainly result in the constriction of the pulmonary-and broncho-postcapillary venules, together with arteriole dilation. The local manifestations of IgE-triggered anaphylaxis include whealing of the skin (urticaria), diarrhea for food allergies, rhinitis or asthma for pollen allergies, or a generalized anaphylactic shock. IgE reactions are usually measured in vitro using RIA (radioimmunoassay), RIST (radioimmunosorbent test) or RAST (radioallergosorbent test) (see Fig. 2.28 and Fig. 2.29, p. 131f.) Frequent causal agents of IgE allergies in humans include pollen, animal hair, house dust (mites), insect bites and stings, penicillin, and foods. Examples of allergic diseases include local allergic rhinitis and conjunctivitis, allergic bronchial asthma, systemic anaphylactic shock, insect toxin allergies, house dust (mite) and food allergies, urticaria, and angioedemas.

Degranulation of mast cells and basophils can be induced by factors other than the cross-linking of specific IgE antibodies. Such factors include the complement factors C3a and C5a, and pharmacological inducers ("pseudo-allergy!").

Atopic patients suffer severely from allergies. Atopia is genetically conditioned, with a child exhibiting a 50% risk of developing atopy if both parents are allergic, or a 30% risk if only one parent is allergic. The incidence level of atopy within the general population is roughly 10-15%. Atopia correlates with high levels of IgE production, and desensitization refers to attempts to change a TH2 (IgE-producing) response into a TH1 (IgG-favoring) response by means of repeated inoculations or oral doses of allergens (see Fig. 2.14, p. 78). It is likely that increased production of IgG—as opposed to IgE—anti-bodies plays a major role in the success of desensitization. IgE no doubt has an important biological function, probably against ectoparasites, with allergic reactions representing nothing more than an unfortunate side effect of this biological system. Little research has been performed on the nature of the protective function of IgE during parasitic infections (or on the role of eosinophils). However, we do know that mediators released by IgE-triggering of mast cells and basophils cause the smooth intestinal musculature to contract, and in this way facilitate the elimination of intestinal parasites.

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