Abstract 2279 Tick-Talk: α-Gal Gives You an Allergic Shock

Alpha-Galactose (ɑ-Gal) Syndrome is an allergy caused by the Galactose-alpha-1,3 galactose molecule entering the bloodstream. Primarily injected through tick salivary glycoproteins, ɑ-Gal may also be transmitted by other arthropods. This salivary deposition results in anaphylaxis, hives, rashes, nausea and other allergic responses following the ingestion of red meat, dairy and gelatin products, which contain ɑ-Gal. Symptoms arise 2-6 hours after consumption, making diagnosis challenging. When ɑ-Gal is detected by the immune system, pathogen-neutralizing Immunoglobulin M production is overridden to produce Immunoglobulin E (IgE). IgE is an allergen-binding protein that plays a major role in allergen identification. IgE binds to host cells, including various white blood cells via the RI (high affinity) and CD23 (low affinity) regions. Two adjacent cell-bound IgEs bind to the same allergen with cross-linking via the ɑ-Gal binding site (IgE Fab region). An allergic reaction occurs with the activation of IgE, which corresponds with the release of histamine, cytokines, and other mediators from the host cell. The symptoms caused by ɑ-Gal syndrome affects the lives of many people, especially in a world where products containing ɑ-Gal are widespread. However, there are some solutions to this allergy such as immunotherapy, Omalizumab drug (anti-IgE), and genetically-modified GalSafe pigs. By understanding the RI and CD23 binding sites and IgE's role in ɑ-Gal detection, potential solutions may arise to help people overcome this allergic barrier. For this project, the Ashbury College SMART Team with support from the Center for BioMolecular Modeling used Jmol 3D modeling and printing technology to model the Fcε3 A and B region of IgE and FcεRI found on mast and basophil cells. (PDB 2Y7Q).