Grass pollen-specific B-cell receptor and T-cell receptor

Grass pollen-specific B-cell receptors (BCR), IgE, and T-cell receptors (TCR) are the central molecular components of the adaptive immune system that mediate allergic reactions to grass pollen. In sensitized individuals, B cells express BCRs and secrete IgE antibodies that specifically recognize allergens such as Phl p 1 and Phl p 5 from Timothy grass [1]. These IgE molecules bind to high-affinity FcεRI receptors on mast cells and basophils, leading to the release of inflammatory mediators like histamine upon allergen exposure [1]. Simultaneously, TCRs on CD4+ T cells recognize allergen-derived peptides presented by MHC class II molecules, typically driving a Th2-polarized inflammatory response [2]. Therapeutic strategies like allergen immunotherapy (AIT) aim to modulate these receptors by inducing peripheral T-cell tolerance and promoting the production of blocking IgG4 antibodies that compete with IgE for allergen binding [3][4]. Monoclonal antibodies, such as Omalizumab, target the IgE component directly to prevent its interaction with effector cells, thereby reducing the allergic cascade [4]. Understanding the repertoire and signaling of these receptors is crucial for developing precision treatments for seasonal allergic rhinitis and asthma.

Other names

Grass pollen-specific IgEAllergen-specific B-cell receptorAllergen-specific T-cell receptorPhl p-specific receptorsGrass pollen-specific BCR/TCR

Allergen immunotherapy (AIT) induces peripheral T-cell tolerance, shifts the immune response from Th2 to Th1, and promotes the expansion of regulatory T cells (Tregs). It also stimulates B cells to produce allergen-specific IgG4 antibodies, which act as blocking antibodies by competing with IgE for allergen binding. Monoclonal antibodies like Omalizumab bind to free IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils.