Immunoglobulin E specific for Phleum pratense allergen 5 (Phl p 5-specific IgE)

IgE antibodies specific for Phleum pratense allergen 5 (Phl p 5) are primary mediators of Timothy grass pollen allergy, one of the most common causes of seasonal allergic rhinitis and asthma worldwide. Phl p 5 is a major allergen from Timothy grass, recognized by IgE in more than 80% of grass-pollen-allergic individuals, and is often associated with high clinical potency (PMID: 15634301). These specific IgE antibodies function by binding to the Phl p 5 protein and subsequently cross-linking the high-affinity IgE receptor (FcεRI) on the surface of mast cells and basophils. This cross-linking triggers the immediate release of inflammatory mediators such as histamine, leukotrienes, and cytokines, which drive the allergic symptomatic response (PMID: 21464374). In a therapeutic context, these antibodies are targeted indirectly by allergen-specific immunotherapy (AIT), which seeks to shift the immune response toward tolerance, and directly by anti-IgE monoclonal antibodies like omalizumab that sequester free IgE (PMID: 12743354). Measurement of Phl p 5-specific IgE is a standard diagnostic tool used to confirm sensitization and guide the selection of patients for grass-specific immunotherapy.

Other names

Anti-Phl p 5 IgETimothy grass allergen Phl p 5 specific IgEPhl p V specific IgETimothy grass pollen-specific IgE

Omalizumab binds to the Cε3 domain of the IgE molecule, preventing its interaction with the high-affinity FcεRI receptor on mast cells and basophils. Allergen-specific immunotherapy (AIT) induces immune tolerance by promoting regulatory T cell activity and increasing the production of allergen-specific IgG4 antibodies, which act as blocking antibodies to prevent IgE-mediated allergen recognition.