There is no known cure for food allergies with sufferers forced to constantly check the ingredients on food packaging and make enquiries at restaurants before digging into a meal. Even taking such precautions it is almost impossible to avoid all food allergen exposure, especially with children. With even minor exposure having the potential to cause severe or even life threatening reactions in some people, the discovery of a way to turn off the immune system’s allergic reaction to certain proteins in mice, could have implications for the millions of food allergy sufferers worldwide.

Allergic reactions to food occur when the immune system misidentifies an otherwise innocuous food protein as harmful, and then attacks the protein with a ferocity far greater than required. Last year we reported that a team at Duke University discovered it was possible for some people allergic to peanuts to build up a tolerance by slowly giving them higher and higher doses of peanut flour in their food each day. While promising, for this method to remain effective the subjects had to keep a daily dose of peanuts in their diets to maintain the tolerance.


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Now a research team at Johns Hopkins University has discovered that one kind of immune cell in the gastrointestinal tract called lamina propria dendritic cells (LPDC), which are considered the first line of defense for a body’s immune system, expresses a special receptor, SIGNR1, which appears on the cells’ surface and binds to specific sugars.

Test results on mice

In the laboratory, the research team, led by Shau-Ku Huang, Ph.D., a professor of medicine, and Yufeng Zhou, M.D., Ph.D., a postdoctoral fellow in the Division of Allergy and Clinical Immunology at Johns Hopkins University School of Medicine, took a food protein that causes allergies in mice and modified it by adding special sugars.

They hypothesized that, when ingested by the mice, the modified proteins would be able to bind to what are known as the SIGNR1 receptors on the immune system cells. Bound in this way, the immune system would learn to tolerate the modified food protein – and the protein would no longer induce an allergic reaction, even when consumed in its unmodified form.

The mice were fed the modified protein once a day for three days. Five days later, they were fed the protein in its unmodified form. Another group of mice was not fed the modified protein at all. The severity of the allergic response to the unmodified protein – which in the control-group mice tended to be tremors, convulsions and/or death – was significantly decreased in those mice that had been pre-fed the modified protein.

Some still had minor reactions like itchiness or puffiness around the eyes and snout, but none had serious ones. These mice appeared to be desensitized to the food protein, even when it was fed to them in its unmodified form, says Zhou. In this model, SIGNR1 plays a key role in shutting off some responses in the immune cells, but the researchers don’t yet know whether this is the only function of this receptor.

Growing problem

In the U.S., it is estimated that six to eight percent of children under the age of three and nearly four percent of adults have food allergies. And the prevalence of allergies is rising, particularly in the developed world, with children growing up in too sterile an environment thought to be a major contributing factor.

Whatever the reason, if the Johns Hopkins team can confirm that their process in mice can also occur in humans it will provide hope that the body could be trained to tolerate food allergies that lead to roughly 300,000 emergency room visits and 100 to 200 deaths each year in the U.S. alone – and it could also mean that one day I might be able to try a peanut butter sandwich and see what all the fuss is about.

The research team's findings are published online in the journal Nature Medicine.