Pru p 3-specific Immunoglobulin E (Pru p 3 sIgE)

Pru p 3-specific Immunoglobulin E (IgE) refers to the subset of IgE antibodies that specifically recognize Pru p 3, the major non-specific lipid transfer protein (nsLTP) found in peaches (Prunus persica) [1]. This molecule plays a central role in the Mediterranean area as a primary sensitizer for food allergies, often leading to severe systemic reactions including anaphylaxis [2]. Upon exposure to the Pru p 3 allergen, these specific IgE antibodies, which are typically bound to high-affinity receptors (FcεRI) on the surface of mast cells and basophils, trigger the release of inflammatory mediators like histamine [3]. This process is the hallmark of Type I hypersensitivity and is responsible for the clinical symptoms of peach allergy and the broader Lipid Transfer Protein (LTP) syndrome [4]. While Pru p 3-specific IgE is primarily used as a diagnostic biomarker to assess the risk of severe allergic reactions, it is also a functional target for therapeutic interventions [5]. Drugs like omalizumab work by sequestering free IgE, thereby preventing its binding to receptors and reducing the sensitivity to allergens like Pru p 3 [6]. Additionally, allergen-specific immunotherapy (AIT) aims to modulate the immune response to reduce the levels or activity of these specific IgE antibodies while increasing protective IgG4 levels [7]. References: [1] UniProt P81402; [2] WHO/IUIS Allergen Nomenclature; [3] Pastorello et al., J Allergy Clin Immunol 1999; [4] Egger et al., Clin Transl Allergy 2011; [5] Asero et al., Eur Ann Allergy Clin Immunol 2018; [6] Maurer et al., N Engl J Med 2013; [7] Alvaro et al., J Investig Allergol Clin Immunol 2013.

Other names

Anti-Pru p 3 IgEPeach-specific IgEsIgE to Pru p 3

Omalizumab binds to the Cε3 domain of IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils. Allergen-specific immunotherapy (AIT) works by inducing immune tolerance, shifting the response from Th2 to Th1/Treg, and promoting the production of IgG4 blocking antibodies that compete with sIgE for allergen binding.