Birch pollen allergen-specific B-cell receptor (Bet v 1-specific BCR)

Birch pollen allergen-specific B-cell receptors (BCRs) are specialized membrane-bound immunoglobulins on B lymphocytes that recognize specific proteins in birch pollen, primarily the major allergen Bet v 1 (Breiteneder et al., 1989). These receptors are central to the allergic sensitization process, where their activation leads to the production of allergen-specific IgE antibodies (Eckl-Dorna et al., 2019). Upon re-exposure, the allergen cross-links IgE bound to high-affinity receptors on mast cells and basophils, or interacts with BCRs on memory B cells, propagating the allergic inflammatory response (Akdis & Akdis, 2014). Therapeutic interventions often focus on modulating the activity of these B cells through allergen immunotherapy (AIT), which seeks to redirect the immune response toward a tolerant state characterized by the production of neutralizing IgG4 antibodies (Shamji & Durham, 2017). Emerging biological therapies, such as cocktail monoclonal antibodies (e.g., REGN5713/5714/5715), are designed to bind the Bet v 1 allergen with high affinity, effectively masking the epitopes that would otherwise trigger the BCR or IgE-mediated allergic cascade (Orengo et al., 2020). This neutralization prevents the allergen from cross-linking IgE on effector cells, thereby inhibiting the release of histamine and other inflammatory mediators. Monitoring the levels of allergen-specific IgE and IgG4 serves as a key biomarker for assessing the efficacy of these treatments in clinical settings.

Other names

Bet v 1-specific B-cell receptorBirch pollen-specific BCRAnti-Bet v 1 B-cell receptorBirch pollen allergen-specific BCR

Allergen immunotherapy (AIT) induces immune tolerance by promoting the expansion of regulatory B cells and shifting antibody production from IgE to protective IgG4, which acts as a blocking antibody. Monoclonal antibodies (e.g., REGN5713/5714/5715) neutralize the Bet v 1 allergen directly, preventing its binding to the B-cell receptor and surface-bound IgE on effector cells.