Denis Daley
Canadian researchers have pinpointed a new gene associated with peanut allergy, offering further evidence that genes play a role in the development of food allergies and opening the door to future research, improved diagnostics and new treatment options.
The affected gene, called c11orf30/EMSY, is already known to play a role in other allergy-related conditions, such as eczema, asthma, and allergic rhinitis. This study is the first to associate the EMSY locus with food allergy, and these findings suggest that the gene plays an important role in the development of not just food allergy but also general allergic predisposition.
Peanut allergy develops in early life and is rarely outgrown. Roughly 1 per cent of Canadian adults and between 2 per cent and 3 per cent of Canadian children are affected, and the symptoms can be severe, even life-threatening.
The findings, published in The Journal of Allergy and Clinical Immunology, were based on DNA from 850 people with a peanut allergy and nearly 1,000 individuals without a peanut allergy. The team scanned over 7.5 million genetic markers across the DNA through a genome-wide association study, searching for clues to which genes might contribute to an increased risk of developing food allergies. The team also analyzed results from six other genetic studies from American, Australian, German and Dutch populations.
They found that EMSY was associated with an increased risk of both peanut allergy and food allergy, and five other gene locations are also suspected to be involved.
“Food allergy is the result of both genetic and environmental factors, but there are surprisingly few data regarding the genetic basis of this condition,” says senior co-author Denise Daley, an Associate Professor in the Department of Medicine, part of a team supported by AllerGen NCE Inc., the Allergy, Genes and Environment Network. “The discovery of this genetic link gives us a fuller picture of the causes for food allergies, and this could eventually help doctors identify children at risk.”