Immunoglobulin E specific for Acacia dealbata pollen allergens (sIgE (Acacia dealbata))

Immunoglobulin E (IgE) antibodies specific for Acacia dealbata pollen allergens are the key immunological mediators of allergic sensitization and clinical symptoms associated with Silver Wattle pollen exposure. These antibodies are generated by the immune system in response to specific allergenic proteins, such as the profilin Aca d 1, found in the pollen of Acacia dealbata (WHO/IUIS Allergen Nomenclature Database). When an sensitized individual is re-exposed to the pollen, these specific IgE molecules, which are bound to high-affinity FcεRI receptors on mast cells and basophils, cross-link with the allergens. This cross-linking triggers the immediate release of inflammatory mediators, including histamine and leukotrienes, resulting in symptoms of allergic rhinitis, conjunctivitis, and asthma (Bousquet et al., 2020). In clinical practice, these specific IgE antibodies serve as diagnostic biomarkers to confirm sensitization. They are also the functional targets of allergen-specific immunotherapy (AIT), which aims to induce immune tolerance and promote the production of protective IgG4 antibodies (Akdis & Akdis, 2014). Additionally, the biological activity of these antibodies can be neutralized by anti-IgE monoclonal antibodies like Omalizumab, which prevents IgE from binding to its receptors on effector cells (Galli & Tsai, 2012).

Other names

Silver wattle pollen-specific IgEAnti-Acacia dealbata IgEAcacia dealbata-specific IgEIgE anti-Aca d 1

Omalizumab is a recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E (IgE). It binds to the Cε3 domain of free IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on the surface of mast cells and basophils, thereby inhibiting the release of inflammatory mediators (Galli & Tsai, 2012). Allergen-specific immunotherapy (AIT) using Acacia dealbata pollen extracts works by the controlled administration of the allergen to induce peripheral T-cell tolerance, shifting the immune response from a Th2 to a Th1/Treg profile and promoting the production of allergen-specific IgG4 antibodies that act as blocking antibodies to compete with IgE (Akdis & Akdis, 2014).