Researchers have developed an experimental vaccine that successfully protects mice from anaphylaxis, a potentially life-threatening allergic reaction, for at least one year. There is optimism that this vaccine will also be effective in humans.

Anaphylaxis poses a persistent threat to millions worldwide, particularly for individuals allergic to foods like peanuts and shellfish. In the UK alone, around 6% of adults, or about 2.4 million people, are believed to have clinically confirmed food allergies.

Allergic reactions can occur from consuming contaminated food or even from kissing someone who has recently eaten the allergenic food. This triggers a surge of immunoglobulin E (IgE) antibodies, leading to symptoms such as throat swelling, breathing difficulties, and a drop in blood pressure. Despite having an epinephrine auto-injector (like an EpiPen) at hand, many still need emergency treatment, and severe cases may be fatal.

Currently, avoiding allergens is the primary method of prevention, with limited alternatives available. Individuals can consider oral immunotherapy, where the allergen is gradually introduced under supervision to build up tolerance. There is also an anti-IgE monoclonal antibody drug, like omalizumab, which binds to IgE to block allergic responses. However, omalizumab is costly and requires injections every few weeks, sometimes indefinitely.

Recently, Laurent Reber and colleagues at the Toulouse Institute of Infection and Inflammation in France developed a vaccine named IgE-K. This vaccine encourages the immune system to produce antibodies that target IgE, preventing it from attaching to receptors on immune cells and averting severe allergic reactions.

“Our goal was to create a long-term solution, as individuals with food allergies face unintentional exposure at any time, necessitating ongoing protection,” says Reber.

In experiments with mice engineered to produce the human variant of IgE, the team discovered that two doses of the vaccine led to the generation of neutralizing antibodies against IgE.

“It blocks the molecules responsible for allergic reactions,” says Josh Koenig from McMaster University in Ontario, Canada.

Upon exposing the mice to a substance that triggered an allergic reaction, the unvaccinated mice experienced significant reactions, while the vaccinated mice exhibited no symptoms and were shielded from anaphylaxis for up to a year.

“It might last longer, but we have yet to conduct further testing,” noted Reber.

IgE forms part of the immune system, activated in response to toxins and certain intestinal parasites apart from allergens. “This mechanism is likely an evolutionary adaptation to combat toxins,” suggests Lever.

Lever asserts there is strong evidence supporting the long-term safety of targeting this molecule, as many individuals with severe allergies have been on anti-IgE therapy for years without negative effects. To assess if reducing IgE would diminish the body’s protective response to parasites, further tests were conducted on mice. The results indicated that the vaccine did not hinder their immune response to infections involving mouse feline, a parasitic nematode.

Koenig expresses hope regarding the vaccine’s efficacy in humans. “Research shows that the mouse-generated antibodies attach effectively to human IgE molecules. If humans can produce similar antibodies, there’s a promising chance it will be highly effective.”

Despite this optimism, Lever emphasizes that clinical trials are necessary to assess the vaccine’s safety, effectiveness, and duration in humans. If it can be commercialized, it may provide a cost-effective treatment alternative for individuals with severe allergies, requiring far fewer injections than anti-IgE monoclonal antibodies such as omalizumab.