Abstract
The allergic response is mediated by binding of allergens to specific IgE antibodies attached via IgE receptors to the surface of mast cells and basophils. The binding of allergens by surface IgE causes degranulation resulting in release of histamine and other mediators of inflammation including interleukin (IL)-4, and IL-5. This IgE-mediated response is called the immediate-phase (hypersensitivity) reaction [1], and occurs within seconds to minutes of allergen exposure. The late-phase response results from the secretion of proinflammatory mediators such as leukotrienes and platelet-activating factor [1], occurs 4–24 hours later and is characterized by the infiltration of eosinophils into the site of allergen exposure. These eosinophils are activated in response to immune complexes, Th2 and mast cell mediators, resulting in the release of toxic substances such as major basic protein (MBP) which causes tissue damage [2]. The release of proinflammatory mediators from both the immediate and late responses then lead to pulmonary allergic inflammation.
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© 1998 Springer-Verlag Berlin Heidelberg
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Roman, M., Spiegelberg, H.L., Broide, D., Raze, E. (1998). Gene immunization for allergic disorders. In: Raz, E. (eds) Gene Vaccination: Theory and Practice. Principles and Practice. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-46867-4_11
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DOI: https://doi.org/10.1007/978-3-642-46867-4_11
Publisher Name: Springer, Berlin, Heidelberg
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