Allergen-specific immunoglobulin E (IgE) and B-cell receptors (BCR) recognizing Phleum pratense and Dactylis glomerata pollen allergens (Grass pollen-specific IgE/BCR)

Allergen-specific immunoglobulin E (IgE) and B-cell receptors (BCRs) recognizing Phleum pratense (Timothy grass) and Dactylis glomerata (Orchard grass) are central to the pathophysiology of grass pollen allergy. These receptors specifically bind to major allergens such as Phl p 1, Phl p 5, and Dac g 1, which are prevalent in temperate regions. In allergic individuals, the B-cell receptor mediates the uptake and presentation of these allergens, while secreted IgE primes mast cells and basophils by binding to the high-affinity FcεRI receptor. Subsequent allergen exposure leads to receptor cross-linking and the rapid release of inflammatory mediators, resulting in clinical symptoms of allergic rhinitis and asthma (PMID: 30102132). Therapeutic strategies include the use of anti-IgE monoclonal antibodies like Omalizumab, which sequester free IgE, and allergen-specific immunotherapy (AIT), which induces immunological tolerance (PMID: 12165860). AIT works by promoting the development of regulatory T cells and the production of allergen-specific IgG4 antibodies that block IgE-mediated activation (PMID: 29307430).

Other names

Timothy grass-specific IgEOrchard grass-specific IgEPhl p-specific IgEDac g-specific IgEGrass pollen-specific B-cell receptorAnti-Phl p IgEAnti-Dac g IgE

Omalizumab and ligelizumab neutralize circulating IgE, preventing its binding to the high-affinity FcεRI receptor on mast cells and basophils (PMID: 12165860, PMID: 31618532). Allergen-specific immunotherapy (AIT) uses grass pollen extracts to induce immunological tolerance, characterized by the expansion of regulatory T cells and the production of allergen-specific IgG4 antibodies that compete with IgE for allergen binding (PMID: 29307430).