Human Immunoglobulin E (IgE) specific for Quercus agrifolia pollen epitopes (sIgE (Quercus agrifolia))

Human Immunoglobulin E (IgE) specific for Quercus agrifolia (Coast Live Oak) pollen epitopes is a key mediator of Type I hypersensitivity reactions in sensitized individuals (PMID: 31034315). These antibodies are produced by B cells following exposure to oak pollen allergens, such as the Bet v 1-homologous proteins common in the Quercus genus (UniProt: P18912). The specific IgE molecules bind to high-affinity FcεRI receptors on the surface of mast cells and basophils. Upon re-exposure to Quercus agrifolia pollen, allergen cross-linking of these surface-bound IgE molecules triggers the immediate release of inflammatory mediators like histamine, proteases, and leukotrienes (PMID: 29370564). This physiological cascade leads to the clinical manifestations of seasonal allergic rhinitis, conjunctivitis, and can exacerbate allergic asthma (NIH: StatPearls - Type I Hypersensitivity). Therapeutic targeting of these IgE antibodies is achieved through monoclonal antibodies like Omalizumab, which sequester free IgE to prevent receptor binding, or through allergen-specific immunotherapy (AIT) using Quercus agrifolia extracts to induce immunological tolerance (PMID: 30219111).

Other names

Coast live oak-specific IgEAnti-Quercus agrifolia IgEQuercus agrifolia allergen-specific IgEOak pollen-specific IgE

Anti-IgE monoclonal antibodies like Omalizumab bind to the Cε3 domain of circulating free IgE, forming small, inactive complexes that prevent IgE from binding to high-affinity FcεRI receptors on mast cells and basophils (FDA: Xolair Label). Allergen-specific immunotherapy (AIT) involves the controlled administration of Quercus agrifolia pollen extracts to shift the immune response from a Th2-mediated IgE production toward a Th1/Treg-mediated response, increasing protective IgG4 levels and inducing long-term desensitization (PMID: 28434611).