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The target comprises the specific IgE antibodies and T-cell receptors (TCRs) that recognize the major allergens of Timothy grass (Phleum pratense), specifically Phl p 1, Phl p 2, Phl p 5, and Phl p 6. These allergens are the primary drivers of seasonal allergic rhinitis (hay fever) and allergic asthma in sensitized individuals, with Phl p 1 and Phl p 5 being particularly potent and widely recognized by over 90% and 65-90% of grass-allergic patients, respectively [11, 12, 16]. Upon exposure, these allergens cross-link IgE bound to high-affinity receptors (FcεRI) on mast cells and basophils, triggering the release of inflammatory mediators, while TCR recognition of allergen-derived peptides promotes a Th2-polarized immune response [2, 9, 12]. Therapeutic strategies targeting these components primarily involve allergen-specific immunotherapy (AIT), which aims to modify the underlying immune response. A prominent example is the recombinant vaccine BM32, which utilizes hypoallergenic peptides from these four allergens fused to a hepatitis B PreS carrier to induce high levels of allergen-specific blocking IgG4 antibodies [2, 4]. These IgG4 antibodies compete with IgE for allergen binding, thereby preventing effector cell degranulation and IgE-facilitated antigen presentation to T cells [2, 9]. Additionally, AIT promotes T-cell tolerance or a shift toward a regulatory T-cell (Treg) or Th1 phenotype, leading to long-term clinical desensitization and disease modification [4, 12].
Induction of allergen-specific blocking IgG4 antibodies, reduction of Th2-mediated T-cell responses, and desensitization of effector cells such as mast cells and basophils.
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