Don’t blame the peanuts, blame transforming growth hormone for your child’s food and environmental allergies.
When it comes to food allergies, peanuts used to be it. Slowly however, the kid who gave away his share of peanut butter cups became the norm. According to the
Allergies were once thought to be a reaction to a child’s environment or upbringing, but researchers at the Johns Hopkins Children’s Center and the Johns Hopkins Institute of Genetic Medicine have uncovered a genetic glitch that they suspect is the basis for allergic diseases.
Researchers focused on patients with Loeys-Dietz syndrome (LDS), a genetic disorder that also makes patients more likely to develop allergies. They found that a signaling molecule called transforming growth factor-β (TGFβ) kick-starts immune responses if it sends signals incorrectly.
TGFβ affects immune cells called regulatory T cells, which usually help keep the body from overreacting to safe substances like food and pet dander. In children with allergies and those with LDS, these T cells actually do the opposite, causing a greater allergic reaction.
So, if multiple allergies stem from just one misbehaving protein molecule, it may be possible to find a single, direct fix for childhood allergies.
“It was interesting to learn that an alteration in a single pathway in people lead to such diverse allergic phenotypes, including asthma, food allergy, eczema, and…gastrointestinal disease,” study author Harry Dietz, M.D., a professor of medicine and genetics at Johns Hopkins, told Healthline.
However, “more work needs to be done to define the exact mechanism by which mutations in the TGFβ receptor perturb immunologic maturation and tolerance,” Dietz said. This study is just the first step, but it’s akin to finding a map to the ultimate anti-allergy drug.
“Prior work in mouse models has suggested that low TGFβ activity can induce a tendency for loss of immune tolerance,” Dietz said. In this study, researchers found a connection between allergies and inflammation and a cellular signature for high TGFβ signaling.
Essentially, the balance of TGFβ signaling in response to food and environmental allergens is very delicate, and too little or too much can result in an allergic reaction.
The study included 58 children with LDS between the ages of 7 and 20, most of whom had a history of allergies, displayed irregular TGFβ signaling, and had high levels of traditional allergic disease markers like white blood cells. Researchers suspect that their findings in LDS patients can be expanded to included more allergic diseases in the general population.
“While these studies instill hope that new therapeutic strategies for allergic disease are on the horizon, it is essential to determine the best ways to achieve a productive balance in TGFβ signaling,” Dietz said.