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August 5, 2019

JAX allergy research might lead to new treatments

Courtesy / Jackson Laboratory Adam Williams and Stephanie Eisenbarth, at Bar Harbor’s Jackson Laboratory for Genomic Medicine, have discovered a cause of severe allergic reactions. The discovery might help with the development of targeted treatments.

Bar Harbor-based Jackson Laboratory says it's part of a research team that has discovered the cellular process that creates a “super-antibody” driving severe allergic reactions, a finding that may lead to new biotechnology treatments.

The research team was co-led by Adam Williams of the Jackson Laboratory for Genomic Medicine and Stephanie C. Eisenbarth of Yale School of Medicine, according to a news release.

The super-antibody is called “high-affinity IgE.” It triggers the most severe allergic reactions, including potentially life-threatening anaphylaxis, which may involve sudden drops in blood pressure, breathing trouble and dizziness.

 The team identified a type of immune cell it believes is the driver, and the research was recently published in Science magazine.

The finding may represent an alternative therapeutic target to prevent or reduce severe allergic reactions, including anaphylaxis.

“If we can identify the cellular players that drive production of high-affinity IgE, then we can understand what's initiating the allergy,” Williams said in the release. “Then, down the line, maybe we can prevent or reverse the generation of this high-affinity IgE,” thereby reducing the severity of allergic reactions.

Mouse assist

The researchers made their discovery by focusing on a genetic disorder, called DOCK8 immunodeficiency. 

Patients with this disease are susceptible to recurrent staphylococcus and viral infections and, despite their immunodeficiency, typically have high levels of IgE and severe food allergies.

The researchers generated a mouse model of DOCK8 deficiency. The mice developed the same high IgE levels as humans and the IgE caused anaphylaxis.

Using the mice, the scientific team found the immune cell and cellular “messenger” system that told the cell to make high-affinity IgE. When the researchers deleted those immune cells in the DOCK8-deficient mice, the symptoms of the disease disappeared.  

The researchers discovered elevated levels of the same immune cell in people with food or respiratory allergies. 

The new work points the way to more precise allergy testing as well as identifying new approaches for treating allergy, according to the release.

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