Immunoglobulin E specific for Quercus alba pollen allergens (sIgE (Quercus alba))

Immunoglobulin E (IgE) antibodies specific for Quercus alba (White Oak) pollen allergens are key effectors in the pathogenesis of oak-induced allergic diseases (Source: WHO/IUIS Allergen Nomenclature). These antibodies are produced by B cells upon sensitization to white oak pollen proteins, particularly the major allergen Que a 1, which belongs to the pathogenesis-related protein family 10 (PR-10) (Source: UniProt P83308). When an individual is re-exposed to the pollen, these specific IgE molecules, which are bound to high-affinity receptors (FcεRI) on mast cells and basophils, recognize and bind the allergens (Source: StatPearls). This recognition causes receptor cross-linking, leading to the immediate release of inflammatory mediators such as histamine, leukotrienes, and cytokines that drive the symptoms of allergic rhinitis and asthma. Therapeutic interventions targeting this pathway include monoclonal antibodies like Omalizumab that neutralize circulating IgE and allergen-specific immunotherapy (AIT), which modifies the underlying immune response to reduce the production and activity of these specific antibodies (Source: Mayo Clinic). Due to the structural similarity of Que a 1 to other PR-10 proteins, these IgE antibodies often exhibit cross-reactivity with allergens from birch and other Fagales trees (Source: JACI).

Other names

White oak-specific IgEAnti-Que a 1 IgEQuercus alba-specific IgEOak pollen-specific IgEsIgE to White Oak

Anti-IgE monoclonal antibodies bind to the Fc region of circulating IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on effector cells (Source: PubChem). Allergen-specific immunotherapy (AIT) involves the administration of increasing doses of Quercus alba allergens to induce immunological tolerance, characterized by the production of allergen-specific IgG4 blocking antibodies and a reduction in the IgE/IgG4 ratio (Source: AAAAI).