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The immune response to Betula verrucosa (Silver Birch) pollen allergens is a Type I hypersensitivity reaction primarily driven by the major allergen Bet v 1 (UniProt: P15494). Bet v 1 belongs to the pathogenesis-related protein family 10 (PR-10) and is responsible for sensitization in over 90% of birch pollen-allergic individuals (Biedermann et al., 2019). Upon inhalation, these allergens cross-link IgE antibodies bound to FcεRI receptors on mast cells and basophils, triggering the release of histamine, leukotrienes, and cytokines. This inflammatory cascade results in clinical symptoms such as allergic rhinitis, conjunctivitis, and exacerbation of asthma (Bousquet et al., 2020). A significant feature of this response is the cross-reactivity between Bet v 1 and homologous proteins in various foods, leading to oral allergy syndrome (Geroldinger-Simic et al., 2011). Therapeutic management involves allergen-specific immunotherapy (ASIT), which utilizes standardized birch pollen extracts to induce immunological tolerance by promoting a shift from Th2 to Th1/Treg responses (Shamji & Durham, 2017). Other pharmacological interventions include the use of H1-antihistamines, corticosteroids, and anti-IgE monoclonal antibodies to manage symptoms and prevent severe reactions.
Allergen-specific immunotherapy (ASIT) induces immunological tolerance by shifting the T-cell response from Th2 to Th1/Treg and increasing allergen-specific IgG4 levels. Symptomatic treatments involve H1-receptor antagonism, topical corticosteroid-mediated anti-inflammation, and IgE neutralization.
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