Grass pollen allergen-specific immunoglobulin G (IgG) and B-cell receptor (BCR) (Grass pollen-specific IgG/BCR)

Grass pollen allergen-specific IgG/IgG4 and B-cell receptors (BCRs) are central mediators in the pathophysiology and treatment of seasonal allergic rhinitis (Shamji et al., 2011, J Allergy Clin Immunol). In sensitized individuals, B-cell receptors specific for grass allergens, such as those from Phleum pratense, facilitate the uptake and presentation of these proteins, leading to the production of allergen-specific IgE. Allergen immunotherapy (AIT) targets these components by repeatedly exposing the immune system to controlled doses of the allergen to induce immunological tolerance (Akdis & Akdis, 2014, Nat Rev Immunol). This process promotes a class switch in B cells from IgE to IgG4 production, creating "blocking antibodies" that compete with IgE for allergen binding sites. These IgG4 antibodies effectively prevent the cross-linking of IgE on mast cells and basophils, thereby inhibiting the release of histamine and other inflammatory mediators. Additionally, AIT modulates BCR signaling to favor the development of regulatory B cells (Bregs) that secrete anti-inflammatory cytokines like IL-10. Drugs interacting with this system include sublingual tablets like Grastek and Oralair, which are FDA-approved for the treatment of grass pollen-induced allergic rhinitis (FDA, 2014). Monitoring the levels of these specific immunoglobulins and the expansion of specific B-cell clones serves as a vital biomarker for evaluating the clinical efficacy and long-term success of immunotherapy.

Other names

Grass pollen-specific IgG4Grass pollen-specific B-cell receptorBlocking antibodiesPhleum pratense-specific IgGTimothy grass-specific immunoglobulin

Induction of allergen-specific IgG4 blocking antibodies and modulation of B-cell receptor signaling to promote immunological tolerance and prevent IgE-mediated mast cell degranulation.