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T-cell receptors (TCRs) and B-cell receptors (BCRs) recognizing grass pollen allergoid epitopes are the primary immunological targets in allergen-specific immunotherapy (AIT) (Pfaar et al., 2019). Allergoids are allergens chemically modified, typically with glutaraldehyde or formaldehyde, to reduce IgE-binding capacity while preserving T-cell immunogenicity (Zidarn et al., 2012). This modification enhances safety by minimizing the risk of IgE-mediated anaphylaxis during treatment (Akdis & Akdis, 2014). When these allergoids interact with BCRs and are presented to TCRs, they trigger a shift from a pro-allergic Th2 profile to a regulatory (Treg) or Th1-dominant profile (Moingeon, 2013). This process leads to the production of blocking antibodies, such as IgG4, which compete with IgE for allergen binding (Shamji & Durham, 2017). Ultimately, targeting these receptors with allergoids induces long-term clinical tolerance to grass pollens, effectively treating allergic rhinitis and asthma (Klimek et al., 2015). These receptors are highly specific to the epitopes presented by the modified grass pollen proteins, such as those from Phleum pratense. The therapeutic goal is to desensitize the immune system by modulating the signaling through these specific receptor populations.
Allergoids bind to B-cell receptors to induce protective IgG4 antibodies and are processed by antigen-presenting cells to interact with T-cell receptors, promoting a shift from Th2 to Th1/Treg responses and inducing immunological tolerance.
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