Scientists supported by the National Institute of Allergy and Infectious Diseases (NIAID) have devised a new, experimental approach to treating allergic diseases. In mice, the scientists used a genetically engineered molecule to connect two receptors on the key immune system cells that cause allergic reactions. Cross-linking these receptor molecules short-circuited the type of allergic reaction that leads to asthma, allergic rhinitis, and even the potentially deadly anaphylaxis caused by food allergy.
This work represents an entirely new approach to treating allergic diseases, says NIAID Director Anthony S. Fauci, M.D. 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 NIAIDs continued support of research into the mechanisms of allergy will lead to other innovative concepts like this one.
This research does what science is supposed to do, says Marshall Plaut, M.D., chief of NIAIDs Allergic Mechanisms Section. The researchers succeeded in translating a scientific observation into a clever therapeutic idea. Details of this work, performed by a team of scientists at the University of California at Los Angeles (UCLA) and the University of New Mexico, appear in the May issue of Nature Medicine.
The scientists designed and created a molecule called GE2 that acts on two types of immune system cells central to allergic reactions: mast cells and basophils. In people with allergies, these cells respond to ordinarily harmless substances, such as pollen or peanut proteins, by releasing chemicals such as histamine that trigger the symptoms of allergic reactions. Histamine, for example, causes swelling, sneezing, itching, and irritation.
GE2 binds to receptor molecules on mast cells and basophils that control the release of histamine. One of these receptor molecules is like a gas pedal: it makes the allergic reaction go.
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Contact: Jeff Minerd
jminerd@niaid.nih.org
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
30-Apr-2002