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Immunoglobulin E (IgE) antibodies specific for Parietaria judaica allergens are the primary mediators of Type I hypersensitivity reactions to the pollen of the Mediterranean weed Parietaria judaica, commonly known as pellitory-of-the-wall (D'Amato et al., 1992, Allergy). These antibodies are produced by B cells upon sensitization and subsequently bind to the high-affinity IgE receptor (FcεRI) located on the surface of mast cells and basophils. When the individual is re-exposed to Parietaria allergens, such as the major allergens Par j 1 and Par j 2 (UniProt P55958, P55959), these proteins cross-link the receptor-bound IgE, triggering cellular degranulation and the release of inflammatory mediators like histamine. This physiological response results in clinical manifestations including allergic rhinitis, allergic conjunctivitis, and bronchial asthma. Therapeutic interventions targeting this pathway include omalizumab, which sequesters free IgE to prevent receptor binding (FDA, Xolair Label), and allergen-specific immunotherapy (AIT), which aims to modulate the immune system toward tolerance (Bousquet et al., 1998).
Omalizumab binds to the Cε3 domain of circulating IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils (FDA, Xolair Label). Allergen-specific immunotherapy (AIT) involves controlled exposure to Parietaria allergens to induce immune tolerance, increase IgG4 blocking antibodies, and shift the response from Th2 to Th1/Treg profiles (Bousquet et al., 1998).
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