Allergic reactions in the skin can be caused by many different chemical compounds found in creams, cosmetics, and other topical consumer products, but how they trigger the reaction has remained somewhat mysterious.
A new study suggests the way some chemicals displace natural fat-like molecules (called lipids) in skin cells may explain how many common ingredients trigger allergic contact dermatitis, and encouragingly, suggests a new way to treat the condition.
The study was led by researchers at Columbia University Irving Medical Center, the Brigham and Women’s Hospital, and Monash University and published online today in Science Immunology.
Why some chemicals trigger dermatitis is a mystery
Poison ivy is a commonly known trigger for allergic contact dermatitis, an itchy skin rash. But many ingredients found in nonprescription topical products can trigger a similar type of rash.
An 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.
Skin cells unmask allergy-inducing chemicals
De Jong and her colleagues suspected that CD1a, a molecule that’s abundant on Langerhans cells (immune cells in the skin’s outer layer), might be responsible for making these chemicals visible to T cells.
In the current study, conducted with human cells in tissue culture, the researchers found 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.
These chemicals included Balsam of Peru and farnesol, which are found in many personal care products, such as skin creams, toothpaste, and fragrances. Within Balsam of Peru, the researchers identified benzyl benzoate and benzyl cinnamate as the chemicals responsible for the reaction, and overall they identified more than a dozen small chemicals that activated T cells through CD1a.
Read the full story on news-medical.net
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