Abstract
Atopic diseases are genetically determined disorders which affect approximately 20%–30% of the general population in developed countries and whose prevalence is increasing over the last decades. They are characterized by an enhanced ability of B lymphocytes to produce IgE antibodies in response to certain groups of otherwise innocuous environmental antigens that can activate the immune system after inhalation or ingestion, and perhaps after penetration through the skin (allergens). Allergen-specific IgE antibodies bind indeed to high affinity (type I) Fcε receptors (FcεRI) present on the surface of mast cells/basophils and allergen-induced FcεRI cross-linking results in the release of vasoactive mediators, chemotactic factors and cytokines that in turn trigger the “allergic cascade” (Lichtenstein 1993). In addition to IgE-producing B cells and IgE-binding mast cells/basophils, eosinophils are also involved in the pathogenesis of atopic diseases, inasmuch as these cells accumulate in the sites of allergic inflammation and the toxic products they release significantly contribute to the induction of tissue damage (Gleich et al. 1994). In the past few years, the cellular basis for the regulation of IgE antibody production has been discovered. More importantly, the intense study on the functional properties of helper T (Th) cells that collaborate with B cells for the synthesis of IgE antibodies has allowed clarification of the mechanisms accounting for the joint involvement of IgE-producing B cells, mast cells/basophils and eosinophils.
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Parronchi, P., Maggi, E., Romagnani, S. (1999). Redirecting Th2 Responses in Allergy. In: Coffman, R.L., Romagnani, S. (eds) Redirection of Th1 and Th2 Responses. Current Topics in Microbiology and Immunology, vol 238. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-09709-0_3
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