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Exciting Breakthrough for the Treatment of Allergic Conditions: The GE2 Molecule A recent study conducted by scientists at the University of California, Los Angeles (UCLA) and by the University of New Mexico (UNM), concludes that an experimental therapy has succeeded in halting allergic reactions in mice. Their findings are reported in the in the May 2002 issue of Nature Medicine and supported by the National Institute of Allergy and Infectious Diseases (NIAID). According to Anthony S. Fauci, M.D., Director of NIAID, "The prevalence of allergic disease has increased significantly in recent decades, and there simply are not many promising therapeutic strategies out there. We hope that NIAID's continued support of research into the mechanisms of allergy will lead to other innovative concepts like this one." The UCLA-UNM study group used a specially designed molecule, GE2, to link two receptors on the key immune system cells that trigger allergy reactions. They discovered that the process of cross-connecting these two receptor molecules effectively "short-circuits" the types of symptoms that can result in the onset of asthma, hay fever and, in extreme cases, life-threatening anaphylaxis. Fauci concludes: "This work represents an entirely new approach to treating allergic diseases." His observations are endorsed by Marshall Plaut, M.D., Chief of NIAID's Allergic Mechanisms Section, who states: "This research does what science is supposed to do . . . the researchers (have) succeeded in translating a scientific observation into a clever therapeutic idea." The GE2 molecule acts on two types of immune cells—mast cells and basophils—both of which are central to allergic reactions. GE2 works by binding itself to the receptor molecules on the mast cells and basophils, thus controlling the release of histamine, which can trigger a reaction in allergy sufferers. Senior study author, Andrew Saxon, M.D., director of the UCLA Asthma, Allergy, and Immunologic Disease Center, offers the following graphic analogy: "One of these receptor molecules is like a gas pedal: it makes the allergic reaction go. The other receptor molecule is like a brake. However, in this case, the brake only works when coupled with the gas pedal. Therefore, we constructed GE2 so that one end 'steps on' the brake while the other end binds to the gas pedal. This cross-linking slows or stops the allergic reaction". The conclusion? The application of GE2 significantly reduced allergic skin reactions, in tests on mice. Further, in laboratory tests on human mast cells and basophils, a clear pattern emerged: the higher the dose of GE2, the lower the level of histamine released by cells stimulated by an allergen. The implications? As research into GE2 therapy is still in its infancy, wider animal trials will be required before this innovative approach can be tested on humans. The possibilities, however, for treating conditions such as asthma, allergic rhinitis (hay fever), chronic urticaria, angioedema, anaphylaxis and other allergic diseases are clearly apparent. Although the current generic structure of the GE2 molecule works indiscriminately to block reactions to all allergens, the potential for refinement and development is immense. Dr. Saxon, for example, proposes the possibility of designing a GE2 to contain a specific allergen targeted at blocking a particular allergic reaction. Much, however, remains to be explored in the area of GE2 therapy for treating allergic diseases. Resource National Institutes of Health. (2002). Experimental therapy stops allergic reactions in mice. Retrieved July 10, 2002, from www.nih.gov/news/pr/apr2002/niaid-30.htm.

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