Allergen-specific B-cell receptor and soluble allergen-specific immunoglobulin (Allergen-specific BCR/Ig)

Allergen-specific B-cell receptors (BCRs) and their secreted counterparts, soluble immunoglobulins (IgE, IgG, and IgA), are the primary mediators of the adaptive immune response to allergens (PMID: 30121073). In allergic individuals, B cells are skewed toward producing IgE, which binds to mast cells and basophils, triggering inflammatory mediator release upon allergen re-exposure (PMID: 29307320). Conversely, allergen-specific IgG (particularly IgG4) and IgA act as blocking antibodies that compete with IgE for allergen binding, thereby inhibiting the allergic cascade (PMID: 31078179). Therapeutic strategies target these molecules either by neutralizing soluble IgE (e.g., omalizumab) or by using allergen immunotherapy (AIT) to reprogram B cells to favor the production of protective IgG and IgA over pathogenic IgE (PMID: 24565705). Understanding the balance between these antibody classes and the signaling of their parent BCRs is critical for developing effective treatments for allergic rhinitis, asthma, and food allergies (PMID: 28434687).

Other names

Allergen-specific BCRAllergen-specific IgEAllergen-specific IgG4Allergen-specific IgAsIgEsIgGsIgA

Anti-IgE antibodies like omalizumab bind to the Cε3 domain of soluble IgE, preventing its interaction with high-affinity FcεRI receptors on mast cells and basophils (PMID: 29307320). Allergen immunotherapy (AIT) induces a class switch in B cells from IgE to IgG4 and IgA, which act as blocking antibodies to prevent allergen-IgE complexes from forming (PMID: 31078179). Additionally, AIT modulates B-cell receptor (BCR) signaling to promote the expansion of regulatory B cells (Bregs) and the induction of long-term immunological tolerance (PMID: 30121073).