Abstract
Type I allergy is an immunologically-mediated hypersensitivity disease with complex genetic background affecting almost 25% of the population (Kay, 1997; Lockey and Bukantz, 1998). As a major feature of their disease, allergic patients produce IgE antibodies against per se mostly harmless antigens (i.e., allergens) which, after allergen-binding, can activate effector and inducer cells of the atopic immune response (Ravetch and Kinet, 1991; Beaven and Metzger, 1993; Bieber, 1996; Stingi and Maurer, 1997). Depending on the site and duration of allergen contact and the type of immune cells involved, the manifestations of Type I allergy may greatly vary (e.g., allergic rhinitis, conjunctivitis, asthma, dermatitis, gastrointestinal disease). Progress made in the field of molecular allergen characterization has revealed that calcium-binding proteins from many sources are frequent targets for IgE antibodies of allergic patients and thus can act as widely spread elicitors of Type I allergy (Valenta et al., 1998). Calcium-binding allergens from different sources share sequence and structural similarities. Therefore, patients who are cross-sensitized to calcium-binding allergens can exhibit allergic symptoms after exposure to many allergen sources. Calcium-depletion experiments indicate that IgE antibodies of sensitized individuals recognize preferentially the calcium-bound forms of the allergens whereas the apoforms are poorly recognized. This fact opens possibilities to employ genetic engineering and synthetic peptide chemistry for the production of hypoallergenic apoforms which may be used for therapeutic vaccination against Type I allergy with a reduced rate of anaphylactic side effects.
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Valenta, R., Twardosz, A., Swoboda, I., Hayek, B., Spitzauer, S., Kraft, D. (2000). Calcium-Binding Proteins in Type I Allergy: Elicitors and Vaccines. In: Pochet, R., Donato, R., Haiech, J., Heizmann, C., Gerke, V. (eds) Calcium: The Molecular Basis of Calcium Action in Biology and Medicine. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0688-0_22
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