Researchers from Columbia University Irving Medical Center explore whether the skin condition can be stopped by using competing lipids that trigger a reaction
Scientists from Columbia University Irving Medical Center, US, are investigating how to stop contact dermatitis from developing on the skin.
Contact dermatitis, an itchy skin rash, begins when the immune system’s T cells recognise a chemical as foreign.
However, research has identified that a chemical reaction with larger proteins needs to take place in order to be picked up by T cells.
Assistant Professor Annemieke de Jong and her colleagues at Columbia University believe CD1a, a molecule found on Langerhans cells, residing on the basal and suprabasal layers of the epidermis, could be the catalyst for making foreign chemicals visible to T cells.
According to the team’s research, several common chemicals known to trigger allergic contact dermatitis were able to bind to CD1a molecules including benzyl benzoate and benzyl cinnamate, found in Balsam of Peru, and farnesol.
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.”
She also quoted work from Monash University, Australia, which showed that farnesol can hide inside CD1a’s tunnel-like interior, displacing the lipids that normally protrude from the CD1a molecule.
“This displacement makes the CD1a surface visible to the T cells, causing an immune reaction,” added de Jong.
This raises the possibility that contact dermatitis could be stopped by applying competing lipids to the skin that displace those triggering the immune reaction.
She continued: “From previous studies, we know the identity of several lipids that can bind to CD1a but won’t activate T cells.”
Contact dermatitis can be managed by using topical ointments to soothe rashes and oral anti-inflammatory agents in severe cases.