A new study suggests the way some chemicals found in cosmetic products displace natural fat-like molecules in skin cells may explain how common ingredients may potentially trigger allergic contact dermatitis.
The study, led by researchers at the Columbia University Irving Medical Center in New York, the Brigham and Women’s Hospital in Boston and Monash University in Australia, was published online ahead of print in Science Immunology (Jan. 3, 2020).
The allergic reaction begins when the immune system’s T cells recognize a chemical as foreign. T cells do not directly recognize small chemicals, and research suggests that these compounds need to undergo a chemical reaction with larger proteins in order to make themselves visible to T cells.
“However, many small compounds in skincare products that trigger allergic contact dermatitis lack the chemical groups needed for this reaction to occur,” said Dr. Annemieke de Jong, the study’s co-leader, in a press release. Dr. de Jong is an assistant professor of dermatology at Columbia University Vagelos College of Physicians and Surgeons.
“These small chemicals should be invisible to T cells, but they’re not.”
Researchers suspect that CD1a, a molecule that is abundant on Langerhans cells, might be responsible for making these chemicals visible to T cells.
The study, which was conducted using human cells in tissue culture, showed that several common chemicals known to trigger allergic contact dermatitis were able to bind to CD1a molecules on the surface of Langerhans cells and activate T cells.
The common chemicals included Balsam of Peru and farnesol, which are regularly found in many personal care products, such as skin creams, toothpaste and fragrances. In Balsam of Peru, the researchers identified benzyl benzoate and benzyl cinnamate as the chemicals responsible for the reaction.
Overall, the study identified more than a dozen small chemicals that activated T cells through CD1a.
“Our work shows how these chemicals can activate T cells in tissue culture, but we have to be cautious about claiming that this is definitively how it works in allergic patients,” Dr. de Jong said. “The study does pave the way for follow-up studies to confirm the mechanism in allergic patients and design inhibitors of the response.”
Structural work done at Monash University showed that farnesol can hide inside the tunnel of CD1a, displacing the natural lipids that normally protrude from the CD1a molecule.
“This displacement makes the CD1a surface visible to the T cells, causing an immune reaction,” said Dr. de Jong.
The discovery made by researchers at Monash University raises the possibility that allergic contact dermatitis reactions could be stopped by applying competing lipids to the skin to displace those triggering the immune reaction.
“From previous studies, we know the identity of several lipids that can bind to CD1a but won’t activate T cells,” Dr. de Jong said.
The only way to avoid allergic contact dermatitis currently is to identify and avoid contact with the offending chemical.
Topical ointments can help soothe the rashes, which usually clear up in less than one month. In severe cases, physicians may prescribe oral corticosteroids, anti-inflammatory agents that suppress the immune system, increasing the risk of infections and other side effects.
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