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Allergen-specific Immunoglobulin E (IgE) to Artemisia annua pollen proteins is a specialized class of antibodies that mediate allergic reactions to the Sweet Wormwood plant. These antibodies are produced by B cells following sensitization to specific pollen proteins, most notably the major allergen Art a 1, a defensin-like protein (Gao et al., 2022, Frontiers in Allergy). Once produced, these IgE molecules bind to high-affinity FcεRI receptors on mast cells and basophils; subsequent exposure to the pollen causes allergen-mediated cross-linking of the IgE, leading to the explosive release of inflammatory mediators such as histamine and leukotrienes (Galli & Tsai, 2012, Nature Medicine). This physiological response is the hallmark of Type I hypersensitivity and manifests clinically as seasonal allergic rhinitis, conjunctivitis, and exacerbations of asthma. Therapeutic management often involves the use of Omalizumab, a humanized monoclonal antibody that targets the Fc region of free IgE to prevent its attachment to effector cells (NCBI PubChem, 2024). Additionally, allergen-specific immunotherapy (AIT) is used to desensitize patients by gradually exposing them to Artemisia annua extracts, thereby reducing the levels of specific IgE and increasing protective IgG4 antibodies (Pfaar et al., 2014, Allergy).
Anti-IgE monoclonal antibodies bind to the Fc region of free IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils. Allergen-specific immunotherapy (AIT) involves the administration of pollen extracts to induce immune tolerance and the production of IgG4 blocking antibodies.
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