Researchers from Duke University have discovered the mechanisms that make rush desensitization techniques work for allergy sufferers. Exposing patients to very low doses of an allergen over time can reduce or even eliminate allergic reactions. The findings, just published in the Journal of Clinical Investigation, may aid in the development of new treatments for serious allergies.
Rush desensitization is a form of immunotherapy commonly used to help patients with allergies. The technique involves giving people low doses of the allergen in a controlled environment. The low doses don’t set off allergic reactions and can be increased over time, helping the patient build up immunity. While rush desensitization has proven to be effective, scientists weren’t sure how it worked.
The research team focused their attention on mast cells. Mast cells are white blood cells filled with granules that contain histamine and other inflammatory compounds. When a patient is exposed to an allergen, the body produces antibodies called immunoglobulins. These antibodies bind to the allergens and then attach themselves to the mast cells. This reaction triggers the mast cell to release the granules that cause allergy symptoms.
The team studied the effects of rush desensitization on laboratory mice. They found that when the mice were exposed to allergens, tiny actin filaments in the mast cells would break down and move to the middle of the cell. This would allow for the expulsion of inflammatory granules. When the mice were exposed to very low allergen doses, however, the actin would break down and move to the center of the cell too early. This movement wasn’t enough to trigger the release of granules and allergy symptoms were suppressed.
The team’s findings provide new insights into the mechanisms responsible for the effectiveness of rush desensitization. The authors believe that this new information can be used to develop better treatments for patients with severe or life-threatening allergies.
W.X. Gladys Ang et al. Mast cell desensitization inhibits calcium flux and aberrantly remodels actin. Journal of Clinical Investigation (2016).