Immunoglobulin E specific for Elaeagnus angustifolia pollen allergens (sIgE (Elaeagnus angustifolia))

Immunoglobulin E (IgE) antibodies specific for Elaeagnus angustifolia pollen allergens are the primary mediators of Type I hypersensitivity reactions in individuals sensitized to the Russian olive tree (Bousquet et al., 2001). These antibodies are produced by B cells in response to specific protein components of the pollen, such as the profilin Ela a 1, the thaumatin-like protein Ela a 2, and the lipid-transfer protein Ela a 3 (WHO/IUIS Allergen Nomenclature). Once produced, these specific IgE molecules bind to high-affinity FcεRI receptors on the surface of mast cells and basophils, effectively priming these cells for activation (Gould & Sutton, 2008). Upon subsequent exposure to Russian olive pollen, the allergens cross-link the surface-bound IgE, triggering the rapid release of inflammatory mediators like histamine, which causes symptoms of allergic rhinitis, conjunctivitis, and asthma (Kustar et al., 2022). Therapeutic interventions include the monoclonal antibody Omalizumab, which neutralizes circulating IgE, and allergen-specific immunotherapy (AIT), which uses pollen extracts to induce immunological tolerance (Akdis & Akdis, 2014). Monitoring the levels of these specific IgE antibodies is essential for both the diagnosis of Russian olive allergy and the assessment of treatment efficacy (Sastre, 2010).

Other names

Russian olive pollen specific IgEAnti-Elaeagnus angustifolia IgEIgE to Ela a 1IgE to Ela a 2IgE to Ela a 3Russian olive allergen-specific IgE

Omalizumab acts by binding to the Cε3 domain of free circulating IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils, thereby inhibiting the allergic cascade (Gould & Sutton, 2008). Allergen-specific immunotherapy (AIT) involves the controlled administration of Elaeagnus angustifolia pollen extracts to induce peripheral T-cell tolerance, promoting a shift from a Th2 to a Th1 immune response and increasing the production of blocking IgG4 antibodies, which compete with IgE for allergen binding (Akdis & Akdis, 2014).